Core Topics in Cardiothoracic Critical Care

Cambridge University Press
978-1-107-13163-7 — Core Topics in Cardiothoracic Critical Care

Edited by Kamen Valchanov , Nicola Jones , Charles W. Hogue
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Core Topics in Cardiothoracic

Critical Care
© in this web service Cambridge University Press www.cambridge.org

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Core Topics in Cardiothoracic

Critical Care
Second Edition
Edited by
Kamen Valchanov
Papworth Hospital
Nicola Jones
Papworth Hospital
Charles W Hogue
Northwestern University in Chicago

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Contents
List of Contributors page ix
Foreword xv
Nick Fletcher
Preface to the Second Edition xvii
Link between Cardiothoracic Anaesthesia and
Intensive Care: Which Patients are Admitted
to Critical Care? xix
Andrew Klein
Scoring Systems and Prognosis xxiii
Allanah Barker and Sam Nashef
List of Abbreviations xxix
Section 1 – Diagnosis 9 Chest Drainage 70

Alia Noorani and Yasir Abu-Omar
1 History and Examination 1
Lachlan Miles and Joseph E Arrowsmith 10 Cardiac Pacing and Defibrillation 77
Sérgio Barra and Patrick Heck
2 Electrocardiography 7
David Begley 11 Arterial and Venous Catheterisation and
Invasive Monitoring 86
3 Echocardiography in the Cardiothoracic Stuart A Gillon, Nicholas A Barrett and
Intensive Care Unit 15 Christopher IS Meadows
Ghislaine Douflé and Andrew Roscoe
4 Coronary Angiography 22
Unni Krishnan and Stephen P Hoole Section 3 – Therapeutic Intervention
5 Bronchoscopy in the Cardiothoracic 12 Antibiotics in the Cardiothoracic Intensive
Intensive Care Unit 28 Care Unit 95
Sumit Chatterji and Pasupathy Sivasothy Oana Cole and Olly Allen
6 Microbiology Testing 38 13 Blood Products and Transfusion 107
A Ruth M Kappeler and Margaret I Gillham Martin Besser
7 Radiology for Cardiothoracic 14 Fluid Administration 116
Intensivists 44 Vasileios Zochios and Kamen Valchanov
Kristian H Mortensen, Peter A Barry and
Deepa Gopalan 15 Inotropes and Vasopressors 123
Gabriel Kleinman, Shahzad Shaefi and
Charles Shayan
Section 2 – Practical Procedures
16 Sedation and Analgesia 130
8 Airway Management in Cardiothoracic
Lachlan Miles and Barbora Parizkova
Intensive Care: Intubation and
Tracheostomy 59 17 Mechanical Ventilation 142
Martin John and Christiana Burt Anja Schneider and Erik Ortmann

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Contents
18 Renal Replacement Therapy 149 30 Systemic Hypertension in Cardiothoracic

Jonah Powell-Tuck, Matt Varrier and Marlies Critical Care 263
Ostermann Antonio Rubino and Susan Stevenson
19 Nutritional Support for Cardiac Surgery and 31 Pulmonary Hypertension in the
Intensive Care 157 Cardiothoracic Intensive Care Unit 272
Peter Faber Mark Toshner and Joanna Pepke-Zaba
20 Physiotherapy and Rehabilitation 164 32 The Infected Patient 278
Adam Baddeley and Allaina Eden Simon J Finney
33 Seizures 285
Ari Ercole and Lara Prisco
Section 4 – Advanced Organ Support
34 The Acute Abdomen in the Cardiac
21 Percutaneous Mechanical Circulatory
Intensive Care Unit 294
Support 173
Simon JA Buczacki and Justin Davies
Evgeny Pavlushkov and Marius Berman
35 Cardiothoracic Trauma 301
22 Ventricular Assist Devices (VAD) 180
Alia Noorani and Ravi J De Silva
Harikrishna M Doshi and Steven SL Tsui
36 The Bleeding Cardiac Surgical
23 Cardiac Extracorporeal Membrane
Patient 307
Oxygenation 193
Jerrold H Levy, Kamrouz Ghadimi and
Jason M Ali and David P Jenkins
Ian J Welsby
24 Respiratory Extracorporeal Membrane
Oxygenation in the Cardiothoracic Intensive
Care Unit 202 Section 6 – Perioperative Care:
Darryl Abrams and Daniel Brodie
The Patient Post Cardiac Surgery
37 Management after Coronary Artery
Section 5 – Acute Disorders Bypass Grafting Surgery 313
Sam Nashef and Paolo Bosco
25A Resuscitation after Adult Cardiac
Surgery 211 38 Intensive Care Unit Management
Jonathan H Mackay Following Valve Surgery 317
Yasir Abu-Omar and Shakil Farid
25B Out-of-Hospital Cardiac Arrest Patients
in the Cardiothoracic Intensive Care 39 Pulmonary Endarterectomy Patients in
Unit 220 Cardiothoracic Critical Care 324
Lisen Hockings and Sophia Fisher Choo Yen Ng
26 Airway Emergencies 231 40 Heart Transplantation 333
Tom P Sullivan and Guillermo Martinez Stephen J Pettit and Anna Kydd
27 Chest Pain as a Symptom on the 41 Lung Transplantation 340
Cardiothoracic Intensive Care Unit 241 JS Parmar
Will Davies
42 Aortic Surgical Patients in the Intensive
28 Acute Dyspnoea and Respiratory Care Unit 347
Failure 247 Pedro Catarino and Swetha Iyer
Ken Kuljit Parhar
43 Thoracic Surgical Patients 356
29 Shock in the Cardiothoracic Intensive Care J Irons and S Ghosh
Unit 256
Fabio Guarracino and Rubia Baldassarri
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Contents
Section 7 – Disease Management 52 Difficult to Wean from Mechanical

Ventilation Patients in the Cardiothoracic
in the Cardiothoracic Intensive Care Intensive Care Unit 434
Unit: Incidence; Aetiology; Diagnosis; Michael G Davies
Prognosis; Treatment
44 Respiratory Disorders: Acute Respiratory Section 8 – Provision and Delivery of
Distress Syndrome 365 Cardiothoracic Intensive Care
Alastair Proudfoot and Charlotte Summers
53 Cardiothoracic Critical Care Nursing,
45 Cardiovascular Disorders: the Heart Failure Outreach and Follow-up 441
Patient in the Intensive Care Unit 372 Jo-anne Fowles
Anna Kydd and Jayan Parameshwar
54 Systems and Processes in Cardiothoracic
46 Neurological Aspects of Cardiac Surgery 380 Critical Care 445
Max S Damian James Moore and Alain Vuylsteke
47 Postoperative Delirium 392 55 Clinical Information Systems 449
Makeida B Koyi, Joseph G Hobelmann and Matthew Jones
Karin J Neufeld
56 Medical Law and Ethics in the Cardiothoracic
48 Haematological Disorders and Cardiothoracic Intensive Care Unit 456
Intensive Care 402 Oana Cole
Jerrold H Levy, Kamrouz Ghadimi and
Ian Welsby 57 Training in Cardiothoracic Intensive
Care 462
49 Pregnancy and Cardiovascular Disorders 408 Amy Needham and Chinmay Padvardthan
Kiran Salaunkey
50 Paediatric Cardiac Intensive Care 418
Ajay Desai, Lidia Casanueva and Duncan Macrae
Exercise Answers 467
51 Grown-up Congenital Heart Disease (GUCH)
Index 471
Patients in the Cardiothoracic Intensive Care
Unit 427
Colour plates are to be found between
Susanna Price and Niki Walker
pages 230 and 231.
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Contributors
Darryl Abrams Peter A Barry

Department of Medicine, Columbia University Department of Surgery, Royal Marsden Hospital,
College of Physicians and Surgeons, New York, London, UK
NY, USA
David Begley
Yasir Abu-Omar Department of Cardiology, Papworth Hospital,
Department of Surgery, Papworth Hospital, Cambridge, UK
Cambridge, UK
Jason M Ali Marius Berman

Department of Surgery, Papworth Hospital, Department of Surgery, Papworth Hospital,
Cambridge, UK Cambridge, UK
Olly Allen Martin Besser
Department of Pathology, Papworth Hospital, Department of Pathology, Papworth Hospital,
Joseph E Arrowsmith Paolo Bosco

Department of Anaesthesia and Intensive Care, Department of Surgery, Papworth Hospital,
Papworth Hospital, Cambridge, UK Cambridge, UK
Adam Baddeley
Department of Physiotherapy, Papworth Hospital, Daniel Brodie
Cambridge, UK Department of Medicine, Columbia University
College of Physicians and Surgeons, New York,
Rubia Baldassarri NY, USA
Department of Anaesthesia and Critical Care
Medicine, Azienda Ospedaliero Universitaria Pisana, Simon JA Buczacki
Pisa, Italy Department of Surgery, Addenbrooke’s Hospital,
Cambridge, UK
Allanah Barker
Department of Surgery, Papworth Hospital, Christiana Burt
Cambridge, UK Department of Anaesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK
Sérgio Barra
Department of Cardiology, Papworth Hospital, Lidia Casanueva
Cambridge, UK Great Ormond Street Hospital, London, UK
Nicholas A Barrett Pedro Catarino

Department of Intensive Care, Guy’s and St Thomas’ Department of Surgery, Papworth Hospital,
NHS Foundation Trust, London, UK Cambridge, UK
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Contributors
Sumit Chatterji Simon J Finney

Department of Medicine, Addenbrooke’s Hospital, Department of Intensive Care, Barts Heart Central,
Cambridge, UK St Bartholomew’s Hospital, London, UK
Oana Cole Sophia Fisher
Department of Anaesthesia and Intensive Care, Department of Anaesthesia, Flinders Medical Centre,
Papworth Hospital, Cambridge, UK Adelaide, South Australia, Australia
Max S Damian Jo-anne Fowles

Department of Neurology, Addenbrooke’s Hospital, Department of Anaesthesia and Intensive Care,
Cambridge, UK Papworth Hospital, Cambridge, UK
Kamrouz Ghadimi
Justin Davies
Department of Anesthesiology, Duke University
Department of Surgery, Addenbrooke’s Hospital,
Hospital, Durham, NC, USA
Cambridge, UK
S Ghosh
Michael G Davies Department of Anaesthesia and Intensive Care,
Department of Respiratory Medicine, Papworth Papworth Hospital, Cambridge, UK
Hospital, Cambridge, UK
Margaret I Gillham
Will Davies Department of Pathology, Papworth Hospital,
Department of Cardiology, Papworth Hospital, Cambridge, UK
Cambridge, UK
Stuart A Gillon
Ajay Desai Department of Intensive Care, Guy’s and St Thomas’
Department of Paediatric Intensive Care, Royal NHS Foundation Trust, London, UK
Brompton and Harefield NHS Foundation Trust,
London, UK Deepa Gopalan
Department of Radiology, Imperial College,
Harikrishna M Doshi London, UK
Department of Surgery, Papworth Hospital,
Cambridge, UK Fabio Guarracino
Department of Anaesthesia and Critical Care
Ghislaine Douflé Medicine, Azienda Ospedaliero Universitaria Pisana,
University Health Network, University of Toronto, Pisa, Italy
Toronto, Ontario, Canada
Patrick Heck
Allaina Eden Department of Cardiology, Papworth Hospital,
Department of Physiotherapy, Papworth Hospital, Cambridge, UK
Cambridge, UK
Joseph G Hobelmann
Ari Ercole Department of Psychiatry, Johns Hopkins
Department of Anaesthesia, Addenbrooke’s Hospital, University School of Medicine, Baltimore,
Cambridge, UK MD, USA
Peter Faber Lisen Hockings

Department of Anaesthesia, Aberdeen Royal Department of Intensive Care, The Alfred Hospital,
Infirmary, Aberdeen, UK Melbourne, Victoria, Australia
Shakil Farid Charles W Hogue

Department of Surgery, Papworth Hospital, Department of Anesthesiology, Northwestern
Cambridge, UK University Feinberg School of Medicine, Chicago, USA

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Contributors
Stephen P Hoole Jerrold H Levy

Department of Cardiology, Papworth Hospital, Department of Anesthesiology, Critical Care and
Cambridge, UK Surgery, Duke University School of Medicine,
Durham, NC, USA
J Irons
Department of Anaesthesia and Intensive Jonathan H Mackay
Care, Papworth Hospital, Cambridge, UK Department of Anaesthesia and Intensive Care,
Swetha Iyer
Department of Surgery, Papworth Hospital, Duncan Macrae
Cambridge, UK Department of Paediatric Intensive Care, Royal
Brompton and Harefield NHS Foundation Trust,
David P Jenkins London, UK
Cambridge, UK Guillermo Martinez
Department of Anaesthesia and Intensive Care,
Martin John Papworth Hospital, Cambridge, UK
Papworth Hospital, Cambridge, UK Christopher IS Meadows
Department of Intensive Care, Guy’s and St Thomas’
Matthew Jones NHS Foundation Trust, London, UK
Judge Business School, University of Cambridge,
Cambridge, UK James Moore
Nicola Jones Papworth Hospital, Cambridge, UK
Deptartment of Anesthesia and Intensive Care,
Papworth Hospital, Cambridge, UK Kristian H Mortensen
Department of Radiology, Great Ormond Street
A Ruth M Kappeler Hospital, London, UK
Department of Pathology, Papworth Hospital,
Cambridge, UK Lachlan Miles
Andrew Klein Papworth Hospital, Cambridge, UK
Papworth Hospital, Cambridge, UK Sam Nashef
Gabriel Kleinman Cambridge, UK
Department of Anesthesiology, Northwestern
Amy Needham
University, Chicago, IL, USA
Makeida B Koyi Papworth Hospital, Cambridge, UK
Department of Psychiatry, Johns Hopkins Karin J Neufeld
University School of Medicine, Baltimore, Department of Psychiatry, Johns Hopkins University
MD, USA School of Medicine, Baltimore, MD, USA
Unni Krishnan Choo Yen Ng
Department of Cardiology, Papworth Hospital, Department of Surgery, Papworth Hospital,
Anna Kydd Alia Noorani

Department of Transplantation, Papworth Hospital, Department of Surgery, Papworth Hospital,
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Contributors
Erik Ortmann Alastair Proudfoot

Department of Anesthesia and Intensive Care, Department of Perioperative Medicine,
Kerckhoff-Klinic, Heart and Lung Centre, Bad St. Bartholomew’s Hospital, London, UK
Nauheim, Germany
Andrew Roscoe
Marlies Ostermann Department of Anaesthesia and Intensive Care,
Department of Intensive Care, Guy’s and St Thomas’ Papworth Hospital, Cambridge, UK
NHS Foundation Trust, London, UK
Antonio Rubino
Chinmay Padvardthan Department of Anaesthesia and Intensive Care,
Department of Anaesthesia and Intensive Care, Papworth Hospital, Cambridge, UK
Kiran Salaunkey
Jayan Parameshwar
Department of Transplantation, Papworth Hospital,
Cambridge, UK
Ken Kuljit Parhar Anja Schneider
Department of Critical Care Medicine, University of Zentrum für Akute und Postakute Intensivmedizin
Calgary, Calgary, Alberta, Canada Kreisklinik Jugenheim, Seeheim-Jugenheim,
Germany
Barbora Parizkova
Department of Anaesthesia and Intensive Care, Shahzad Shaefi
Papworth Hospital, Cambridge, UK Department of Anesthesiology, Northwestern
Js Parmar
Department of Transplantation, Papworth Hospital, Charles Shayan
Cambridge, UK Department of Anesthesiology, Northwestern
Evgeny Pavlushkov
Department of Surgery, Papworth Hospital, Ravi J De Silva
Cambridge, UK Department of Surgery, Papworth Hospital,
Joanna Pepke-Zaba Cambridge, UK
Department of Respiratory Medicine, Papworth
Hospital, Cambridge, UK Pasupathy Sivasothy
Department of Medicine, Addenbrooke’s Hospital,
Stephen J Pettit Cambridge, UK
Department of Transplantation, Papworth Hospital,
Cambridge, UK Tom P Sullivan
Jonah Powell-Tuck
Department of Intensive Care, Guy’s and St Thomas’
NHS Foundation Trust, London, UK Charlotte Summers
Susanna Price University of Cambridge School of Clinical
Department of Intensive Care, Royal Brompton and Medicine, Cambridge, UK
Harefield NHS Foundation Trust, London, UK
Susan Stevenson
Lara Prisco Department of Anaesthesia and Intensive Care,
Department of Anaesthesia, Addenbrooke’s Hospital, Papworth Hospital, Cambridge, UK
Cambridge, UK
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Contributors
Mark Toshner Alain Vuylsteke

Department of Respiratory Medicine, Papworth Department of Anaesthesia and Intensive Care,
Hospital, Cambridge, UK Papworth Hospital, Cambridge, UK
Steven SL Tsui Niki Walker

Department of Surgery, Papworth Hospital, Department of Intensive Care, Royal Brompton and
Cambridge, UK Harefield NHS Foundation Trust, London, UK
Kamen Valchanov Ian Welsby

Deptartment of Anesthesia and Intensive Care, Department of Anesthesiology, Duke University
Papworth Hospital, Cambridge, UK Hospital, Durham, NC, USA
Matt Varrier Vasileios Zochios

Department of Intensive Care, Guy’s and St Thomas’ Department of Anaesthesia and Intensive Care,
NHS Foundation Trust, London, UK Papworth Hospital, Cambridge, UK
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Foreword
I am very pleased to be able to provide a brief intro- up and, combined with a very eminent US academic,
duction to the owner, borrower or reader of this text. revisited, reorganised and rewritten the problems and
This book is an update of the successful 2008 Core solutions in this area of practice. Kamen Valchanov
Topics in Cardiothoracic Care text. When that book and Nicola Jones have taken over the authorship
was published, it was the first to provide a detailed from their mentors at the world leading Papworth
insight into the cardiothoracic critical care unit and Hospital and have produced a book that retains the
was widely read and appreciated. Since then other vision and wisdom of the original and added the
authors have produced texts that explore this fascin- significant advances in knowledge, technology and
ating area of practice, but none have quite replicated practice. A significant positive change is the addi-
that originality and quality. . . until now! tion of Professor Charles Hogue of Johns-Hopkins,
Cardiac critical care evolved quite separately Baltimore and Northwestern University, Chicago for
from general intensive care. It essentially originated a North American perspective. Knowing them all, it
as a side room on the cardiac surgical ward in the is not in the least surprising that they have produced
1950s where the patient who struggled after cardiac a book of such scope and such high quality. The con-
surgery was ventilated and cared for by the cardiac tributing authors are all experts in their fields and are
anaesthetist and surgeon. Today we have large mul- drawn from a wide international base.
tidisciplinary teams in large technology dominated This book will prove invaluable to the critical care
purpose-built tertiary units. This has been a rapid nurse, the trainee anaesthetist, surgeon and intensiv-
and hugely successful evolution. Cardiothoracic criti- ist. It will also be of value to the new and established
cal care is now a full blooded and highly influential consultants who are involved with patients with car-
subspecialty in the ever expanding critical care field. diothoracic disease, which extends well beyond the
Indeed I firmly believe that where cardiac intensivists bounds of surgery now. I feel proud to have been
tread today, general intensivists will follow tomorrow. invited to write this foreword and I am proud to fully
This evolution has been accompanied by a vast expan- recommend this work.
sion in research and regulation. No branch of medi-
cine is so scrutinised and yet so open to new thinking Nick Fletcher
and new solutions. The link between cardiothoracic Consultant in Cardiothoracic and Vascular Critical Care
anaesthesia and cardiothoracic critical care is vital in St George’s University Hospital, London UK
the joined up care of these complex patients, as is the
close link with all the related specialties such as the Past President of the Association for Cardiothoracic
surgeon, the cardiologist, the echocardiographer and Anaesthesia and Critical Care (UK)
so many more.
We are fortunate that the new generation of critical
care doctors and authors from Papworth have stepped
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Preface to the Second Edition
Why the second edition of Core Topics in Cardio- How do we practise in this specialty? We pro-
thoracic Critical Care? The first edition of Core Topics vide organ support to patients who have undergone
in Cardiothoracic Critical Care was published in 2008. cardiothoracic surgery or who have failing cardiac
It has been a great success, providing a comprehen- or respiratory function, with the hope that they will
sive text for the specialty and selling so many paper respond to treatment and survive. However, these
copies that Cambridge University Press had to reprint days with modern advances in life support technol-
the book to meet the demands of the market. The first ogy, such as extracorporeal membrane oxygenation,
editors Dr Alain Vuylsteke, Dr Andrew Klein, and Mr death is no longer a binary phenomenon. As guard-
Sam Nashef laid the foundation stone. However, a lot ians of this technology we must be ever mindful of
has happened in the world of medicine since 2008, our patients’ quality of life and the long-term outcome
not least in cardiothoracic critical care. Indeed prac- from our interventions. Importantly we must guard
tice has expanded so much that cardiothoracic critical against sustaining life at all costs and offer patients
care has been recognised as a separate sub-specialty and their loved ones, care which makes them happy,
by the Faculty of Intensive Care Medicine in the UK. or at least acts in their best interests.
Therefore, the current editors were tasked with pro- In 2018 a vast amount of evidence exists to guide
viding an updated version of this textbook, which will this practice. However, it can be challenging to apply
hopefully offer to the reader state-of-the-art informa- evidence from trials to the heterogeneous group of
tion on the current practice in cardiothoracic critical patients we treat in Cardiothoracic Critical Care each
care. with unique, rapidly changing derangements of car-
diorespiratory function. The world of evidence-based
A Few Notes from the Editors medicine is also riddled with problems of spurious
Different sources point to different events as the birth evidence, and an ever-increasing number of articles
of our specialty of intensive care medicine. Most describing scientific trials are being retracted by the
revolve around mechanical ventilation with some publishers. In the end among a myriad of scientific
believing intensive care started in Boston in 1912 when and less scientific articles, guidelines and protocols,
a girl suffering from poliomyelitis received mechani- based on expert opinion, the patient has to be sup-
cal ventilation. Others feel that it is the organised care ported through their critical illness and recovery
for polio victims in need of invasive ventilation that after surgery. In most cases good doctors, nurses and
laid the foundations of the specialty. It is probably a allied healthcare professionals use patient tailored
little easier to define the birth of cardiothoracic criti- approaches in their daily work to provide patients
cal care medicine as this was born when cardiac sur- with the best possible care. We hope that the following
geons needed to leave patients who had undergone text will offer ample and unbiased information to help
heroic operations in a place where they could recover. us work in the best interest of each individual patient.
Similarly to general intensive care medicine we do not
have a specific disease to treat, rather we have very Kamen Valchanov
sick patients with complex disorders of the cardio- Nicola Jones
respiratory system to care for. Charles W Hogue
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Link between Cardiothoracic Anaesthesia and Intensive

Care: Which Patients are Admitted to Critical Care?
Andrew Klein
Introduction cardiac surgery, admission to an ICU will be manda-
tory after anaesthesia. It is reasonable to expect their
Admission to an intensive care area is undertaken
condition to worsen following a period of cardiopul-
for the diagnosis, management and monitoring of
monary bypass, and preparations should be made for
patients with conditions that require close or con-
any necessary organ support, for example use of ino-
stant attention by a group of specially trained health
tropes or haemofiltration.
professionals. Critical care encompasses all areas that
Consideration must also be taken as to whether
provide level 2 and/or level 3 care as defined by the
the patient is appropriate for long-term management
Intensive Care Society document ‘Levels of Critical
on an ICU. An example of this might be a palliative
Care for Adult Patients, 2009’ (Table 1). All level 2
thoracic oncology patient undergoing a procedure for
and level 3 areas have higher staffing levels, special-
symptom relief; such a patient might be more appro-
ist monitoring and more advanced treatment options
priately placed in an HDU with a limit on the medical
available. Level 2 areas are commonly referred to as
interventions that would be appropriate. This manage-
High Dependency Units (HDUs), while level 3 areas
ment plan should be discussed and formulated with
are Intensive Care Units (ICUs), and we will make
the patient and relatives prior to the procedure itself.
this distinction in our text. In some hospitals, the two
are separated geographically, whilst in others they co-
exist in one area. Diagnostic and Surgical Related
It is extremely common for patients undergoing Factors
cardiothoracic interventions under anaesthesia to be A diagnostic model can be utilised in order to pro-
admitted to an ICU or HDU afterwards and this can vide guidelines for admission, which identifies spe-
often be a preplanned decision based on the poten- cific conditions and diseases where it is felt a higher
tial for the patient to become more critically unwell or level of care is always warranted. With respect to car-
unstable. However, given the current pressures placed diothoracic intensive care, the majority of such condi-
on the health service, in terms of both bed occupancy tions will fall under the umbrellas of the cardiac and/
and finances, each individual case should be con- or respiratory systems. However, it is also possible for
sidered and a decision made as to whether such an a patient to require admission on the basis of an addi-
admission will be necessary. These decisions can often tional diagnosis, such as sepsis or a neurological com-
be very difficult and must take into consideration a plication of surgery.
number of factors. All patients undergoing sternotomy will man-
date admission to either an ICU or cardiac recovery
Patient Related Factors environment after their procedure. The differentia-
A patient’s comorbidities, physiological reserve, prog- tion between the two is discussed below. A number
nosis and wishes should all be taken into account of cardiothoracic surgical procedures will always
when planning their most appropriate postoperative warrant ICU admission, due to the complex nature
destination. Prioritisation of patients for critical care of the intervention and often long procedural times.
beds should highlight only those patients likely to gain Examples of these are repair of aortic dissection, or
from an increased level of care and thus not those that multiple valve procedures.
are either too well or too sick to benefit. The majority of patients undergoing thoracic
It is clear that for some high-risk patients, such as surgery will either be admitted to an HDU or dis-
those with known chronic organ failure undergoing charged back to the ward following a period of close
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Which Patients are Admitted to Critical Care?
Table 1 Levels of critical care
Level of Criteria for admission Examples

care
0 General ward • Requires hospitalisation but needs can be met Intraveous drug administration
through normal ward care Observations needed less than 4 hourly
1 Coronary care unit • Recently discharged from higher level care Minimal 4 hourly observations
• In need of additional monitoring/intervention, Continuous oxygen therapy, management of
clinical input or advice epidural, chest drain in situ
• Requiring critical care outreach service Risk of clinical deterioration, high early
support warning score
2 High dependency • Requiring preoperative optimisation Invasive monitoring to optimise fluid balance
unit • Requiring extended postoperative care Major elective surgery, emergency surgery in
• Stepping down to level 2 from level 3 care unstable patient
• Requiring single organ support Minimal hourly observations
• Requiring basic respiratory plus basic Non-invasive ventilation, single intravenous
cardiovascular support vasoactive drug
Continuous oxygen therapy and intra-aortic
balloon pump
3 Intensive care unit • Requiring advanced respiratory support alone Invasive mechanical ventilator support via
• Requiring a minimum of two organ systems endotracheal tube or tracheostomy
supported (except basic respiratory plus basic Acute renal replacement therapy and
cardiovascular – level 2, as above) vasoactive medication
monitoring in recovery after surgery. An HDU bed Admission to an ICU may also depend on the
may often be requested to ensure vigilance in the availability of a required specific treatment for an
immediate postoperative period, and also to allow individual patient. Some centres provide special-
optimisation of pain control. ised advanced organ support, such as extracorporeal
membrane oxygenation. Also, cardiothoracic surgery
Alternative Resources is a high-risk specialty fraught with potential compli-
Each individual institution will have slightly different cations, some of which might require transfer out to
facilities available for the care of their patients and an alternative centre, for example to access neurosur-
these must be taken into consideration when plan- gical intervention.
ning postprocedural care. Early goal-directed ther-
apy and utilisation of a ‘fast-track’ approach has been Time of Admission
adopted successfully in many cardiothoracic centres A well-organised cardiothoracic surgical centre
and this may allow lower risk patients to be admit- should incorporate a robust system of communica-
ted to a cardiac recovery area as a temporary meas- tion with both its ICU and HDU with respect to the
ure postoperatively, before being discharged back to daily admission requirements and bed availability.
a ‘stepdown’ unit or ward. For such systems to work The majority of patients undergoing anaesthesia will
and ensure safe patient care, there must be immedi- require elective admission and surgical activity will be
ate access to critical care and adequate numbers of planned according to such requirements.
trained nursing staff. This model has been proven to However, the ICU and HDU must also always take
be successful in some hospitals and can potentially into account the potential for unplanned emergency
improve patient flow. However, for many institutions admissions, either transferred in for surgical inter-
the safest option remains to admit all cardiac surgical vention, or due to unexpected complications intraop-
patients to the ICU postoperatively. The priority in eratively. Patients should be admitted to the required
such institutions is then to discharge out into a step- higher level of care before their condition reaches a
down unit as soon as possible after extubation and a point from which recovery may be extremely difficult.
period of stability. In reality, it is often much better practice to assume
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Which Patients are Admitted to Critical Care?
a bed will be needed for your patient, than be left in advances in providing ‘fast-track’ surgery, and cardiac
a situation where the availability is not there and the recovery units have become increasingly popular. In
patient is unstable. This could potentially lead to a addition, thoracic surgery does not always necessitate
worsened patient outcome, and may also put unnec- an HDU bed and often an adequate level of care can be
essary pressure on the relevant intensive care unit to provided on general wards with critical care outreach
discharge prematurely. support. Requirements for a higher level of care are by
no means well defined and clinical practice will con-
Conclusion tinue to evolve with time.
It is often assumed that all patients undergoing cardi- Given the current climate in the health care sys-
othoracic surgery will warrant admission to either an tem, with a constant pressure for beds and a drive to
ICU or HDU postoperatively and in many instances improve patient flow, it is extremely important that
that remains the case. Cardiothoracic anaesthesia is a each case undergoing cardiothoracic anaesthesia is
high-risk specialty and it is imperative that the post- considered individually and the safest care for that
operative care system in place in each institution is patient determined. Such planning will take into con-
safe and robust. sideration patient related factors, their diagnosis and
However, variety in admission indications and required surgery and the resources available in the
rates does exist. In recent years there have been institution.
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Scoring Systems and Prognosis

Allanah Barker and Sam Nashef
Crystal Balls • Helping to measure the performance of the

service by comparing actual and predicted
Knowing the likelihood of survival after cardiac
outcomes; and
surgery is useful for multiple reasons including for
weighing the potential risks versus benefits of sur- • Comparing the performance of different
gery. Further, accurate predicting of outcome allows institutions, surgeons and anaesthetists by
for comparison with the actual outcome and thus correcting for risk when outcomes are assessed.
insight into the overall performance of the cardiac Preoperative models take no account of what happens
surgical unit. Knowledge of who is likely to develop in the operating theatre and are therefore less use-
major morbidity also has an impact on the use of valu- ful in predicting which of a number of postoperative
able resources and may allow for sensible planning of patients with complications are likely to emerge intact
operating lists. In addition, some believe that being from the critical care unit.
able to predict mortality with some certitude may help There are probably more risk models in cardiac
clinicians to determine when further efforts are futile. surgery than in any other branch of medicine. Most
Unfortunately, the perfect predictor – a crystal ball to rely on a combination of risk factors, each of which
foresee the future – has not yet been fully developed. is given a numerical ‘weight’. Weights are added,
multiplied or otherwise mathematically processed to
Risk Models or Scoring Systems come up with a percentage figure to predict mortality
Scoring systems allow reasonable prediction of out- or survival. In additive models, the weights given to
come after cardiac surgery. Many models have been the risk factors are simply summed to give the pre-
devised to work out the likelihood of survival, and dicted risk. They are easy to use and can be calculated
these and others have also been shown to predict mentally or ‘on the back of an envelope’. They are less
major morbidity, long-term survival and resource use accurate than more sophisticated systems and have a
with some accuracy. Models can be broadly divided tendency to overscore slightly in low-risk patients and
into two groups: to underscore considerably in very high-risk patients.
Examples of such models are the Parsonnet (the pio-
• Preoperative models, applied before the operation,
neering heart surgery risk model) and the original
with no knowledge of intraoperative events; and
additive EuroSCORE for cardiac surgery overall.
• Postoperative models, applied immediately after
Other models deal specifically with cardiac surgi-
the operation on admission into the critical care
cal subsets, like coronary surgery and valve surgery.
unit, taking some account of what the operation
Sophisticated models use Bayesian analysis, logistic
did to the patient.
regression or even computer neural networks. They
do not allow easy bedside calculation, necessitating
Preoperative Models a computer for determining risk. They are, however,
These are most useful for more stable than additive models across the risk range
• Establishing the risk of surgery as an adjunct and slightly more accurate in exact risk prediction.
to surgical decision making (determining the Examples of such models are the Society of Thoracic
indication to operate on the basis of risk-to- Surgeons (STS) model, the logistic EuroSCORE and
benefit assessment); EuroSCORE II for overall cardiac surgery.
• Providing the patient with information, which is The widespread application of scoring systems
helpful in obtaining consent; in heart surgery has allowed robust performance
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xxvi
measurement and probably contributed to the dra- Extent of Cardiac Disease

matic drop in cardiac surgical mortality seen in the
The severity of coronary disease is subjective and
last 15 years.
therefore not included in surgical risk scores. The
Syntax score allows for a measure of the severity of
Preoperative Model Risk Factors disease, but is time consuming and partly subjective.
Not surprisingly, several common risk factors are Left main stem disease may be associated with more
included in all models (age, gender and left ventricu- risk. Objective measures of cardiac disease include
lar (LV) function). Other risk factors are included in recent myocardial infarction (MI), unstable angina
some models but not in others, such as hypertension, and mechanical complications of MI such as acute
diabetes and obesity. Models also differ depending rupture of the mitral valve or ventricular septum.
on whether they deal with all cardiac surgeries or a
specific subset, such as coronary surgery or valvular Repeat Operation
surgery. They share many risk factors and it would
Previous cardiac surgery (or previous sternotomy)
be repetitive to list them all here, but the models are
increases difficulty of access and prolongs operative
easily accessible and there are interactive calcula-
time. These patients therefore carry an increased risk of
tors available online: www.euroscore.org and http://
bleeding as well as possibly having more advanced dis-
riskcalc.sts.org/stswebriskcalc/. EuroSCORE II also
ease than those undergoing their first cardiac procedure.
offers a smartphone ‘app’ for use at the bedside.
Lung Disease
Age The presence of chronic pulmonary disease such as
There is an increased risk above the age of 60 years. chronic obstructive pulmonary disease (COPD) has a
large impact on how a patient is managed in anaes-
Gender thetic and ventilatory terms. After cardiac surgery,
Females have a higher operative mortality than patients with concurrent lung disease are more likely
males, possibly because of smaller coronary artery to require extended ventilation and to develop pul-
size, smaller blood volume predisposing to risks monary complications, such as chest infections. Lung
associated with perioperative anaemia and transfu- function is difficult to quantify with a single test and
sion, although the definitive reason for the difference severity is based partly on subjective judgements.
is unknown. However, chronic pulmonary disease is taken into
account in the EuroSCORE and STS.
Left Ventricular Function Renal Disease

As estimated by echocardiography or angiography, LV
Renal dysfunction, as evidenced by dependence on
function is a good measure of cardiac status, but deter-
dialysis, increases mortality by as much as 40%, but
mination can be operator dependent and it is difficult
the spectrum of renal failure is wide and difficult to
to produce an accurate and reproducible percentage
quantify. Creatinine levels are easy to measure, but are
ejection fraction. Thus, LV function is generally classi-
not always an accurate measure of true kidney func-
fied as ‘good’, ‘moderate’ or ‘poor’; EuroSCORE II has
tion. The original EuroSCORE uses grossly deranged
an additional category of ‘very poor’.
serum creatinine (>200 μmol/l) as a measure of sig-
nificant renal impairment. Other scores use dialysis
Type of Surgery dependence. The best measure is probably creatinine
General cardiac risk models take into account patients clearance (CC), and this now features in EuroSCORE
that undergo different surgeries – the risk for coro- II, where the categories of renal dysfunction have
nary artery bypass graft (CABG) surgery is less than expanded into four: normal function (CC > 85 ml/
for valve surgery, which in turn is less than that for minute), moderate (CC 50–85 ml/minute), severe
surgery of the thoracic aorta. Combined procedures (CC <50 ml/minute) and on dialysis (regardless of
like valve with CABG carry a higher risk than single CC). Interestingly, patients with severe dysfunction
procedures. but not on dialysis yet fare worst.
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Other Risk Factors Renal

These include peripheral vascular disease, neurologi- As preoperatively, the mainstay of renal function is
cal dysfunction, degree of urgency, diabetes, hyper- serum creatinine level as it is easily measured and a
tension and degree of pulmonary hypertension. In relatively inexpensive test; this variable can be used
addition, various scoring systems give weight to the to monitor changes in renal function and to compare
type of operation performed. current with preoperative function.
Postoperative Models Gastrointestinal/Hepatic
These models benefit from information that is only Both APACHE and SOFA use bilirubin levels as a
available after the completion of the operation, such as measure of liver function. APACHE is used more
the physiological parameters on admission to critical widely in general critical care units and includes
care. Many have been devised for critically ill patients many more variables, such as amylase, albumin (as a
outside the cardiac surgical specialty, but have been rough measure of nutritional status) and other liver
used and validated in cardiac surgery. The most well- function tests. The APACHE score also contains
known models are the Acute Physiology and Chronic variables to measure metabolic function and sep-
Health Evaluation (APACHE) and the Sequential tic status. These criteria are less relevant in cardiac
Organ Failure Assessment (SOFA) (Table 1). The surgery.
APACHE score is used on admission to critical care to
assess the risk of in-hospital death, whereas the SOFA
was developed to quantify the severity of a patient’s ill- Thoracic Surgery
ness using the degree of organ dysfunction at any one Risk modelling is not as developed in thoracic sur-
time. The BRiSc score is specifically aimed at predicting gery, although recently some attempts have been
patients likely to bleed excessively after heart surgery. made to produce models for predicting mortality
after lung resection. The most important risk fac-
tors associated with a poor outcome are age (older
Postoperative Model Risk Factors people do less well) and how much functioning
Postoperative risk scores look at each organ system lung remains long after the resection (the more, the
systematically and score according to derangement of better).
function. Basically, the more organ dysfunction, the
poorer the prognosis.
Learning Points
Respiratory • Many models help to predict the outcome of
Oxygenation and the requirement for ventilatory sup- cardiac surgery, and these can be applied before
port are used as measures of respiratory function. or after the operation.
• Preoperative models help in the decision
making, consent and assessment of clinical
Circulatory performance.
Most scores which are applied postoperatively use mean • Postoperative models can help to plan resource
arterial pressure as an easily measured and monitored use and provide information to relatives.
parameter. However, whereas APACHE concentrates
• Models devised specifically for mortality
on derangement of normal physiology, SOFA concen-
have also been found to be useful in predicting
trates on the need for (and level of) inotropic support.
major morbidity, resource use and long-term
outcomes.
Neurological • No amount of risk modelling can predict with
Trends are more useful than a snapshot at a particular certainty which patient will live and which
point in time, but the Glasgow Coma Scale is easily will die and they should be used as an adjunct
measured and provides an easily reproducible meas- rather than as a replacement for sound clinical
ure of neurological status. judgement.
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Table 1 Postoperative cardiac surgery risk assessment scores
Organ system SOFA APACHE

Respiratory Oxygenation (PaO2/FiO2) Respiratory rate non-ventilated
Respiratory support PaO2 with FiO2 1.0
PaCO2
Coagulation/haematological WCC WCC
Haematocrit
Platelet count
Prothrombin time
Circulatory Mean arterial pressure Mean arterial pressure
Dopamine dose Heart rate ventricular response
Adrenaline dose Central venous pressure
Norepinephrine dose Evidence of acute MI
Dobutamine use Arrhythmia
Serum lactate
Arterial pH
Neurological Glasgow Coma Scale Glasgow Coma Scale
Renal Creatinine Creatinine
Urine ouput/24 hour Urine output/24 hour
Blood urea nitrogen
Gastrointestinal/hepatic Bilirubin Amylase
Albumin
Bilirubin
Alkaline phosphatase
Liver enzymes
Anergy by skin testing
Septic Cerebrospinal fluid positive culture
Blood culture positive
Fungal culture positive
Rectal temperature
Metabolic Calcium level
Glucose
Sodium
Potassium
Bicarbonate
Serum osmolarity
Abbreviations: APACHE, Acute Physiology and Chronic Health Evaluation; FiO2, fraction of inspired oxygen; MI, myocardial infarction;
PaCO2, partial pressure of carbon dioxide in arterial blood; PaO2, partial pressure of oxygen in arterial blood; SOFA, Sequential Organ
Failure Assessment; WCC, white cell count.
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Nashef, SAM, Roques F, Sharples LD, et al. EuroSCORE

Further Reading II. European Journal of Cardio-Thoracic Surgery. 2012;
Arts D, de Keizer NF, Vroom MB, et al. Reliability and 41: 1–12.
accuracy of sequential organ failure assessment. Parsonnet V, Dean D, Bernstein AD. A method of uniform
Critical Care Medicine. 2005; 33: 1988–1993. stratification of risk for evaluating the results of
Knaus WA, Draper EA, Wagner DP, et al. APACHE II: a surgery in acquired adult heart disease. Circulation.
severity of disease classification system. Critical Care 1989; 79: 3–12.
Medicine. 1985; 13: 818–829. Vuylsteke A, Pagel C, Gerrard C, et al. The Papworth
Nashef S. The Naked Surgeon. The Power and Peril of Bleeding Risk Score: a stratification scheme for
Transparency in Medicine. London: Scribe, 2015. identifying cardiac surgery patients at risk of
Nashef SAM, Roques F, Michel PR, et al. European system excessive early postoperative bleeding. European
for cardiac operative risk evaluation (EuroSCORE). Journal of Cardio-Thoracic Surgery. 2011; 39:
European Journal of Cardio-Thoracic Surgery. 1999; 924–930.
16: 9–13.
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Abbreviations
AC Assist-Control ventilation BLUE Bedside Lung Ultrasound in

ACBT Active Cycle of Breathing Technique Emergency
ACEI Angiotensin Converting Enzyme BNP B-type Natriuretic Peptide
Inhibitor BPF Bronchopleural Fistula
ACLS Advanced Cardiac Life Support BPS Behavioural Pain Scale
ACT Activated Clotting Time BTC Bridge to Candidacy
AD Advanced Directive BTS British Thoracic Society
AEDs Automated External Defibrillators BTT Bridge to Transplant
AEG Atrial Electrocardiogram BURP Backwards, Upwards and Rightward
AEP Auditory Evoked Potentials Pressure on the thyroid cartilage
AF Atrial Fibrillation CABG Coronary Artery Bypass Grafting
AFE Amniotic Fluid Embolism CAM-ICU Confusion Assessment Method for the
AKI Acute Kidney Injury ICU
ALG Anti-human Lymphocyte Globulin CAP Community Acquired Pneumonia
ALS Advanced Life Support CC Creatinine Clearance
AMP Adenosine Monophosphate CCA Critical Care Area
APACHE Acute Physiology and Chronic Health CCS Canadian Cardiovascular Society
Evaluation ccTGA Congenitally Corrected Transposition
APRV Airway Pressure Release Ventilation of the Great Arteries
aPTT Activated Partial Thromboplastin CCU Coronary Care Unit
Time CDC Centers for Disease Control
AR Aortic Regurgitation cEEG Continuous Electroencephalography
ARB Angiotensin Receptor Blockers CF Cystic Fibrosis
ARDS Acute Respiratory Distress CHD Congenital Heart Disease
Syndrome CHF Congestive Heart Failure
ARF Acute Respiratory Failure CICO ‘Can’t Intubate, Can’t Oxygenate’
ASD Atrial Septal Defect CIN Contrast Induced Nephropathy
ATG Anti-human Thymocyte Globulin CI Cardiac Index
ATLS Advanced Trauma Life Support CIS Clinical Information Systems
AVNRT Atrioventricular Node Re-entrant CK Creatinine Kinase
Tachycardia CKD Chronic Kidney Disease
AVSD Atrioventricular Septal Defect CLABSI Central Line Associated Bloodstream
BAL Bronchoalveolar Lavage Infections
BALF Bronchoalveolar Lavage Fluid CLAD Chronic Lung Allograft Dysfunction
BIPAP Biphasic or Bilevel Positive Airway CMR Cardiac Magnetic Resonance
Pressure CMV Continuous Mandatory Ventilation
BIPDs Bilateral Independent PDs CMV Cytomegalovirus
BIS Bispectral Index CNI Calcineurin Inhibitors
BiVAD Bilateral Ventricular Assist Device CO Cardiac Output
BLS Basic Life Support
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Abbreviations
COAD Chronic Obstructive Airways Disease, ELSO Extracorporeal Life Support

same as COPD Organisation
COPD Chronic Obstructive Pulmonary EMR Electronic Medical Records
Disease ERP Enhanced Recovery Programmes
CP Constrictive Pericarditis ESBL Extended Spectrum Beta-Lactamases
CPAP Constant Positive Airway Pressure ESG Endovascular stent graft
CPAx Chelsea Critical Care Physical ETT Endotracheal Tube
Assessment Tool EVLWI Extravascular Lung Water Index
CPB Cardiopulmonary Bypass EWMA Exponentially Weighted Moving
CPE Carbapenemase Producing Average
Enterobacteriaceae EWS Early Warning Scores
CPOT Critical Care Pain Observation Tool FAC Fractional Area Change
CPP Cerebral Perfusion Pressure FALLS Fluid Administration Limited by Lung
CRP C-Reactive Protein Sonography
CT Computerised Tomography FAM Functional Assessment Measure
CTCA Computerised Tomography Coronary FB Flexible Bronchoscopy
Angiogram FBC Full Blood Count
CTEPH Chronic Thromboembolic Pulmonary FDO2 Fraction of Oxygen Delivered
Hypertension FEV1 Forced Expiratory Volume for 1
CV Stroke Volume second
CVC Central Venous Catheter FFP Fresh Frozen Plasma
CVD Cardiovascular Disease FIM Functional Independence Measure
CVP Central Venous Pressure FIRDA Frontal IRDA
CXR Chest X-Ray FOUR Full Outline of Unresponsiveness
DAG 1,2-Diacylglycerol FRC Function of Residual Capacity
DBD Donation after Brain Death FS Fraction of Shortening
DBexs Deep Breathing Exercises FVC Forced Vital Capacity
DCD Donation after Circulatory Death GBS Guillain–Barré Syndrome
DD Diastolic Dysfunction GCS Glasgow Coma Score
DNAR Do Not Attempt Resuscitation Order GEDVI Global End-Diastolic Volume Index
DOLS Deprivation of Liberty Safeguards GICS Gastrointestinal Complication Score
DSI Daily Sedation Interruption GPCR G Protein Coupled Receptors
DT Destination Therapy GUCH Grown-Up Congenital Heart disease
DTI Direct Thrombin Inhibitor HD Haemodialysis
DVT Deep Venous Thrombosis HDF Haemodiafiltration
EACA Epsilon Aminocaproic Acid HDU High Dependency Unit
ECC Emergency Cardiovascular Care HES Hydroxyethil Starch
ECCO2R Extracorporeal Carbon Dioxide HF Haemofiltration
Removal HFV High Frequency Ventilation
ECG Electrocardiography HIT Heparin Induced Thrombocytopenia
ECLS Extracorporeal Life Support HIV Human Immunodeficiency Virus
ECMO Extracorporeal Membrane HLHS Hypoplastic Left Heart Syndrome
Oxygenation HOCM Hypertrophic Obstructive
ECPR Extracorporeal Cardiopulmonary Cardiomyopathy
Resuscitation HSV Herpes Simplex Virus
EDA End-Diastolic Area HTEA High Thoracic Epidural Analgesia
EEG Electroencephalography IABP Intra-aortic Balloon Pump
EF Ejection Fraction ICD Implantable
ELISA Enzyme-Linked Immunosorbent Cardioverter-Defibrillators
Assay ICP Intracranial Pressure
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Abbreviations
ICSD Intensive Care Delirium Screening MDT Multidisciplinary Team

Checklist MET Medical Emergency Teams
ICU-AW Intensive Care Unit Acquired MHI Manual Hyperinflation
Weakness MI Myocardial Infarction
IE Infective Endocarditis MIC Minimum Inhibitory Concentration
IJV Internal Jugular Vein MMF Mycophenolate Mofetil
IMCA Independent Mental Capacity MMV Mandatory Minute Ventilation
Advocate mPAP Mean Pulmonary Arterial Pressure
IMV Invasive Mechanical Ventilation MR Mitral Regurgitation
INR International Normalised Ratio MRSA Methicillin Resistant Staphylococcus
INTERMACS Interagency Registry for Mechanically aureus
Assisted Circulatory Support MSE Myoclonic Status Epilepticus
IPF Idiopathic Pulmonary Fibrosis MSSA Methicillin-Sensitive Staphylococcus
IR Interventional Radiology aureus
IRDA Intermittent Rhythmic Delta Activity mTOR Mammalian Target of Rapamicin
IRV Inversed Ratio Ventilation Inhibitors
IS Incentive Spirometry MUST Malnutrition Universal Screening Tool
ISHLT International Society for Heart and MV Mitral Valve
Lung Transplantation NAAT Nucleic Acid-Based Amplification
ITBVI Intrathoracic Blood Volume Index Technologies
IUGR Intrauterine Growth Retardation NAP4 Fourth National Audit Project
IVC Inferior Vena Cava NAVA Neurally Adjusted Ventilatory Assist
IVS Interventricular Septum NCS Non-convulsive Seizures
JET Junctional Ectopic Tachycardia NCSE Non-convulsive Status Epilepticus
LAD Left Anterior Descending artery NHSBT National Health Service Blood and
LAS Lateral Amiotrophic Sclerosis Transfusion
LBBB Left Bundle Branch Block NI Narcotrend Index
LCx Left Circumflex Artery NICE National Institute for Clinical
LMA Laryngeal Mask Airway Excellence
LMCA Left Main Coronary Artery NIPPV Non-invasive Positive Pressure
LMWH Low Molecular Weight Heparin Ventilation
LTACH Long-Term Acute Care Hospitals NIRS Near Infrared Spectroscopy
LV Left Ventricle NIV Non-invasive Ventilation
LVAD Left Ventricular Assist Device NMDA N-Acetyl-D-Aspartate receptor
LVEDV Left Ventricular End-Diastolic Volume NOAC Newer Oral Anticoagulants
LVESV Left Ventricular End-Systolic Volume NRS Nutritional Risk Screening
LVOT Left Ventricular Outflow Tract NVE Native Valve Endocarditis
LVOTO Left Ventricular Outflow Tract NYHA New York Heart Association
Obstruction OD Optical Density
LVSF Left Ventricular Systolic Function OHCA Out-of-Hospital Cardiac Arrest
MACE Major Adverse Cardiac Events OIRDA Occipital IRDA
MALDI Matrix Assisted Laser Desorption/ OpCAB Off pump Coronary Artery Bypass
TOF MS Ionisation Time-of-Flight Mass PAC Pulmonary Artery Catheter
Spectrometry PAH Pulmonary Arterial Hypertension
MAO Monoamine Oxydase PAP Pulmonary Arterial Pressure
MAP Mean Arterial Pressure PAWP Pulmonary Arterial Wedge Pressure
MCCD Mechanical Chest Compression PBM Patient Blood Management
Devices PBW Predicted Body Weight
MCFP Mean Circulatory Filling Pressure PCAS Post-Cardiac Arrest Syndrome
MDR Multidrug Resistance PCI Percutaneous Coronary Intervention
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Abbreviations
PCP Pneumocystis jirovecii Carinii ROTEM Rotational Thromboelastometry

Pneumonia RRT Renal Replacement Therapy
PCR Polymerase Chain Reaction RV Right Ventricle
PCT Procalcitonin RVP Right Ventricular Pressure
PCWP Pulmonary Capillary Wedge Pressure RVAD Right Ventricular Assist Device
PD Peritoneal Dialysis RWMA Regional Wall Motion Abnormalities
PDA Posterior Descending Artery SACP Selective Antegrade Cerebral
PDE Phosphodiesterase Inhibitors Perfusion
PDR Posterior Dominant Rhythm SAH Subarachnoid Haemorrhage
PDs Periodic Discharges SAM Systolic Anterior Motion
PE Pulmonary Embolism SAS Sedation Agitation Scale
PEA Pulmonary Endarterectomy SDD Selective Digestive Decontamination
PEEP Positive End Expiratory Pressure SE Status Epilepticus
PF Pulmonary Fibrosis SGA Subjective Global Assessment
PF4 Platelet Factor 4 SIMV Synchronised Intermittent Mandatory
PFIT Physical Functional Intensive Care Ventilation
Test SLED Slow Low-Efficiency Dialysis
PGD Primary Graft Dysfunction SMR Standardised Mortality Ratio
PH Pulmonary Hypertension, same as SOFA Sepsis Related Organ Failure
PAH Assessment
PKC Protein Kinase C SR Sarcoplasmic Reticulum
PLC Phospholipase C SRA Serotonin Release Assay
PPCs Postoperative Pulmonary SSEP Somatosensory Evoked Potentials
Complications SSRI Selective Serotonin Reuptake Inhibitor
PPCI Primary Percutaneous Coronary SVC Superior Vena Cava
Intervention SVCS Superior Vena Cava Syndrome
PPCM Peripartum Cardiomyopathy SVR Systemic Vascular Resistance
PPHN Persistent Pulmonary Hypertension of TAA Thoracic Aortic Aneurysm
the Newborn TAH Total Artificial Heart
PPV Pulse Pressure Variation TAPSE Tricuspid Annular Plane Systolic
PRC Post-resuscitation Care Excursion
PRES Posterior Reversible Encephalopathy TAPVD Total Anomalous Pulmonary Venous
Syndrome Drainage
PRVC Pressure Regulated Volume TCPC Total Cavopulmonary Connection
Controlled Ventilation TEG Thromboelastography
PSI Patient State Index TETS Transcutaneous Energy Transfer
PT Prothrombin Time Systems
PTE Pulmonary Thromboendarterectomy, TEVAR Thoracic Endovascular Aortic Repair
same as PEA TGA Transposition of the Great Arteries
PTLD Post-transplantation TnC Troponin C
Lymphoproliferative Disorder TNF Tumour Necrosis Factor
PVE Prosthetic Valve Endocarditis TOE Transoesophageal Echocardiography
PVR Pulmonary Vascular Resistance TOF Tetralogy of Fallot
RAP Right Atrial Pressure TPG Transpulmonary Gradient
RASS Richmond Agitation Sedation Scale TR Tricuspid Regurgitation
RBBB Right Bundle Branch Block TRALI Transfusion Related Lung Injury
RCM Restrictive Cardiomyopathy TTE Transthoracic Echocardiography or
RCT Randomised Controlled Trial Thoracic Expansion Exercises as TTEs
ROC Receiver Operating Characteristic TTM Targeted Temperature Management
ROSC Return of Spontaneous Circulation TXA Tranexamic Acid
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Abbreviations
URR Urea Reduction Ratio VT Ventricular Tachycardia

VALI Ventilator Associated Lung Injury VTI Velocity-Time Integral
VAP Ventilator Associated Pneumonia VTM Viral Transport Media
VATS Video Assisted Thoracic Surgery vWF von Willebrand Factor
VF Ventricular Fibrillation WCRS Withdrawal of Cardiorespiratory
VHI Ventilator Hyperinflation Supports
VRE Vancomycin Resistant Enterococci WOB Work of Breathing
VSD Ventricular Septal Defect WPW Wolff–Parkinson–White syndrome
xxxiii

1
Section 1 Diagnosis
History and Examination

Chapter
1 Lachlan Miles and Joseph E Arrowsmith
The first rule of diagnosis, gentlemen!

Eyes: first and most; hands: next and least; tongue:
History
not at all! The Conscious Patient
Sir Lancelot Spratt –as played by James Robertson All available sources of information should be drawn
Justice upon to construct as detailed a history as possible.
In: Doctor in the House (1954, The J. Arthur Rank Where the patient is conscious and able to respond
Organisation) to direct questioning, this important primary source
of information should not be overlooked. Rather
than using ‘open’ questions and expecting them to
Introduction recount their entire current and past medical history
Patients may be admitted to the specialist cardio- in a concise fashion and in chronological order, it is
thoracic critical care unit from a variety of sources often easier to ask the patient to confirm previously
(Figure 1.1). In all elective admissions, and in the documented information and append newly acquired
majority of emergency admissions, a clinical his- information as necessary. When faced with an acutely
tory will already have been elicited and a physical unwell and possibly deteriorating patient, the skilled
examination performed –often more than once. intensivist needs to be able to quickly gather sufficient
Most patients will already have undergone exten- information to aid diagnosis and guide management.
sive investigation or therapeutic intervention, and Of particular importance is the patient’s understand-
the underlying diagnosis or diagnoses will have ing of their medical condition, their insight into treat-
been established. Despite this seemingly ideal situ- ment options and prognosis, and their expectations.
ation, the cardiothoracic intensivist should adopt an Corroborative history from family and carers is also
inquisitive attitude and use the so-called ‘history and invaluable, especially in the setting of acute delirium
physical examination’ to confirm previous findings, or dementia, where the patient’s own account may be
assess disease progression and exclude new path- unreliable. This information should be solicited and
ology. Contrary to popular belief, this is often the documented whenever possible.
most efficient and effective means of predicting and Symptoms of cardiorespiratory disease (e.g.
detecting significant comorbid conditions. Clinical angina pectoris, dyspnoea, orthopnoea, syncope, pal-
investigations should therefore be considered an pitations, ankle swelling, etc.) (Table 1.2) should be
adjunct to, rather than a substitute for, basic medical actively sought, as should any recent progression in
assessment. symptom severity. Symptoms should be described in
In the critical care setting, particularly when a terms of their nature (using the patient’s own words),
patient is physiologically unstable or has reduced con- onset, duration, progression, modifying factors and
sciousness, the conventional stepwise approach to the associations. The impact of symptoms on functional
history and physical examination will usually require status should be documented using the New York
modification (Table 1.1). Indeed it may have to be Heart Association (NYHA) classification and the
conducted during or after initial resuscitation. Canadian Cardiovascular Society (CCS) angina scale.
13:36:26 1
.003
2
Section 1: Diagnosis
Table 1.1 Modification of conventional history and physical for use in critical care
Conventional Critical care

History of presenting complaint Handover information
Past medical history Review of medical notes
Past surgical/anaesthetic history Information from family members
Drug history, allergies, sensitivities
Recreational substance (mis)use
Educational level/native language
History
Social/employment history
Religious/cultural beliefs
Family history
Systematic enquiry
Sensory impairments
Review of medical notes
Patient supine –reclining at 45° Patient supine, lateral or prone
Cardiovascular ABC (Airway, Breathing, Circulation)
Respiratory Lines, tubes, drains and catheters
Physical Gastrointestinal Drug and fluid infusions
Genitourinary Ongoing physiological monitoring
Neurological Anatomical examination
Integument
Airway Intervention Operating Room Emergency

(Bronchoscopy) Suite Department
Critical
External Care High Dependency Unit
Community Unit /Stepdown Unit
Other hospital
Radiology Department Ward/Floor

(Coronary, structural,
electrophysiological)
Figure 1.1 Cardiothoracic critical care admission sources.
Enquiry into the patient’s past medical history respect to the unintubated patient who may require
should include coexisting conditions, previous hospital intervention during their stay, and the patient who is
admissions, surgical procedures and complications, already intubated who will require extubation before
prolonged hospitalisation and unplanned admissions discharge to the ward. Factors known to be associated
to a critical care unit. It is important to note the indi- with increased mortality and morbidity (e.g. con-
cation for any surgical procedure or therapeutic inter- gestive cardiac failure, peripheral vascular disease,
vention (e.g. splenectomy, permanent pacemaker, renal insufficiency, arterial hypertension, pulmonary
angioplasty), the outcome of the procedure and any hypertension, diabetes mellitus, chronic pulmonary
anaesthetic related morbidity. A history of difficult disease, neurological disease and previous cardiovas-
tracheal intubation is of particular note, both with cular surgery) should be documented.
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3
Chapter 1: History and Examination
Table 1.2 Common symptoms associated with Where adherence to a particular cultural or reli-
cardiorespiratory conditions gious belief system (e.g. Jehovah’s Witnesses) has
Cardiovascular Respiratory the potential to influence any aspect of critical care
Syncope Recent overseas travel
management, this should be comprehensively docu-
mented. In some instances it may be appropriate to
Chest pain Fever and/or rigors
explore and document a patient’s specific wishes in a
Fatigue or exercise Facial or sinus pain
number of hypothetical clinical scenarios, including
intolerance
limits of care. It is often preferable that limits of care
Exertional dyspnoea Chest pain
be discussed with the patient and family early on in the
Paroxysmal nocturnal Cough
critical care stay, rather than late in the course of the
dyspnoea
illness when the patient is in extremis. It is important
Orthopnoea Sputum production (volume,
that both the patient and the family have a realistic
time course, purulence)
understanding of what intensive care can offer, rather
Palpitations Haemoptysis
than relying on preconceived ideas.
Intermittent claudication or Dyspnoea
ischaemic rest pain
Stroke or transient Exercise intolerance
The Unconscious Patient
ischaemic attack The unconscious, critically unwell patient represents a
Cough or sputum History of bird keeping, special challenge for any clinician. From a cardiothor-
production asbestos exposure, or other acic point of view, such patients cover a wide range of
sources of occupational lung potential presentations, including, but not limited to
disease
the following:
Peripheral oedema
• A patient transferred from the operating theatre
or catheter laboratory following an invasive
procedure;
Where the patient has been admitted following a
diagnostic or therapeutic intervention (e.g. coronary • A patient admitted following out-of-hospital
angiography or angioplasty), a comprehensive medical cardiac arrest, via either the catheter laboratory or
and nursing ‘handover’ is essential. This is particularly the emergency department;
important when the patient has been brought to hospital • A patient requiring ongoing organ support
by emergency ambulance and taken directly to the angi- following an interventional cardiology or
ography suite. Similarly, when a patient is transferred bronchoscopic intervention; and
from another hospital for specialist cardiothoracic care • A ward patient who has physiologically
(e.g. surgical repair of acute type A aortic dissection), deteriorated and requires more advanced
a formal handover of clinical information and docu- treatment modalities or resuscitation.
mentation is an absolute prerequisite for the transfer of When reviewing an obtunded patient the clinician
clinical responsibility and for safe ongoing care. In many is deprived of many of the usual visual and auditory
areas a formal handover document or aide memoire is clues that guide patient assessment, forcing the use of
used both to guide and to document the comprehensive alternative sources of information. Family members
handover of clinically relevant information. and carers are often the key source of information
It is essential to record current and recent pre- regarding recent symptoms, and it is often possible to
scription drug administration, including formula- establish the temporal course of the presenting com-
tion, dosage and route of administration. In addition, plaint with thorough questioning. In many respects,
the medication history should include drugs taken it is often possible to obtain a full history, provided
‘as required’, proprietary or ‘over-the-counter’ medi- that the right questions are asked, and an open mind
cines, complimentary or alternative therapies, and maintained.
recreational drugs. This latter category should include A thorough review of the medical record is also
alcohol and tobacco products. A history of allergic invaluable when the patient is not able to speak for
or other idiosyncratic reaction to a specific drug (e.g. him or herself. Written correspondence from other
suxamethonium) or class of drugs (e.g. penicillins) clinicians (e.g. surgeons, cardiologists, respiratory
should be sought and documented. physicians, general practitioners) will answer many
13:36:26 3
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4
questions regarding the course of illness leading up The postoperative cardiac or thoracic surgical
to admission. Where questions remain unanswered patient will have a variable number of mediastinal and
regarding the previous clinical course, direct commu- pleural drains in situ. The volume of blood in these
nication with these sources is encouraged, not only to should be recorded so that an accurate estimation of
obtain further information, but as a matter of courtesy any ongoing blood loss can be made. An air leak may
regarding the condition of their patient. also be present when pleural drains are on suction, and
the magnitude and respiratory phase of this should be
Physical Examination judged. Where epicardial pacing wires are present,
their function should be confirmed. If in use, external
The Conscious Patient pacing should be converted from fixed rate mode to
Whilst a comprehensive physical examination is some- demand mode, with an appropriate backup rate.
times not possible given the limitations that reception
and resuscitation of the critically ill patient places on The Hands and Arms
assessment, a full physical examination should never- Examination of the hands reveals much about the
theless be attempted. There is also a frequent tempta- circulatory state of the patient. Cold and shut down
tion for the clinician to rely on the battery of monitors extremities with delayed capillary return may suggest
that an intensive care admission entails, especially a high degree of systemic vascular resistance, usually
during daily review of the patient, or to perform an because of hypovolaemia or low cardiac output state,
investigation rather than seek clinical findings. This is or alternatively, an acutely ischaemic limb. In con-
a fallacy, as even an abbreviated physical examination trast, warm peripheries suggest a normal or high car-
during a ward round may reveal a finding (e.g. bron- diac output state. Finger clubbing may be indicative of
chial breathing) that may take hours to manifest as chronic cardiorespiratory disease, notably congenital,
worsening hypoxia or increasing oxygen requirement, cyanotic heart disease, non-small-cell lung cancer and
permitting early investigation and intervention. suppurative lung conditions such as cystic fibrosis or
bronchiectasis.
General Inspection The peripheral pulses can give clues to the presence
This should initially be undertaken from the end of of significant valvulopathy (e.g. the ‘water hammer’
the bed, so as to better appreciate the overall Gestalt. pulse of severe aortic regurgitation) and regional per-
The initial focus should be on the patient. Central or fusion abnormalities, particularly in aortic dissection
peripheral cyanosis may be evident in the setting of (i.e. radioradial and radiofemoral delay). Inspection
hypoxaemia or shunting. The patient posture proof the palmar creases was popularised for the esti-
vides many important clues, especially when assessing mation of plasma haemoglobin concentration, but
respiratory effort. Pursed lip breathing to increase end- has subsequently proven to be unreliable. Rarely, the
expiratory pressure and a ‘tripod’ position with the immunological and embolic phenomena of infective
shoulders rotated forward and the hands on the lower endocarditis (Janeway lesions and Osler’s nodes) may
extremity to engage the accessory muscles are evidence be evident.
of respiratory distress. Attention should then be turned
to the various drug infusions being administered, the The Neck
relevant concentration, rate and route of administra- Neck examination in the critical care environment
tion. Peripheral and central venous access should be is often difficult, due to the presence of indwelling
noted and recorded including available lumens for jugular venous catheters. In the event that the neck
other medications and the size of each catheter if the is unencumbered, examination of the jugular venous
administration of volume is required. Invasive moni- waveform can be used to assess right atrial filling and
toring (e.g. arterial line, pulmonary artery catheter), compliance, atrioventricular dissociation (cannon a-
circulatory support devices (intra- aortic balloon waves) and torrential tricuspid regurgitation (massive
pump, ventricular assist device and extracorporeal cv-waves). These abnormalities are also visible on the
circuits) and renal replacement therapy should also be central venous waveform if invasive monitoring is
evaluated. An indwelling urinary catheter may be pre- present.
sent, and if so, the volume and concentration of urine If pericardial tamponade is suspected, an early
in the drainage bag should be noted. sign of compromise is an increase in right atrial
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5
Chapter 1: History and Examination
pressure on deep inspiration (Kussmaul’s sign). If the and dorsalis pedis pulses should be sought, particu-
patient’s trachea is not intubated, it is wise to conduct larly if the femoral vessels have been used for arterial
an airway assessment at this juncture if not already access. Whilst a rare event, acute lower limb ischaemia
performed. Auscultation of the carotid arteries may is a recognised complication of a wide range of inva-
reveal bruits consistent with turbulent flow if there is a sive devices, in particular peripheral venoarterial
substantial atheroma burden, or the referred murmur ECMO cannulae and the intra-aortic balloon pump.
of aortic stenosis. It is important to note that even if a distal reperfu-
sion line is incorporated into an ECMO circuit, distal
The Praecordium pulses may be absent. However, the limb should feel
As for other parts of the body, and as alluded to in the warm and well perfused or, at the very least, similar to
starting quotation, examination of the chest should its counterpart.
follow the traditional route of observation, palpation, Deep venous thrombosis is a common compli-
percussion and auscultation. Ideally, both the anterior cation in many postoperative patients, and whilst
and posterior chest should be examined, as the lower at least half of these are completely asymptomatic,
lobes of the lung (particularly on the left) can take up the remainder may exhibit the classical signs of calf
much of the posterior aspect, preventing examination tenderness, swelling, distended superficial veins
of the other lobes if the anterior chest is not examined. and warmth. The traditional test for this condition,
The often high volume of ambient noise in the critical Homan’s sign (rapid passive dorsiflexion of the ankle
care environment may make ausculation challenging. with the aim of causing pain in the calf), is no longer
Subtle abnormalities may be missed, and seemingly recommended because of the risk of clot fragmenta-
positive findings may be misinterpreted. It is wise to tion and acute pulmonary embolism.
correlate findings not consistent with the overall con- Finally, the presence and extent of any peripheral
dition of the patient with appropriate investigation. oedema should be assessed. Oedema is, by definition,
Radiological investigation and bedside modalities an excess of interstitial fluid, and therefore must be the
such as ultrasound and transthoracic echocardiog- result of a derangement of the Starling forces across
raphy are valuable for this purpose. the microcirculation (increased capillary hydrostatic
pressure, decreased plasma colloid oncotic pressure,
The Abdomen increased capillary permeability or deranged lymph-
Initially, at least, the abdomen is rarely a focus in the atic drainage).
cardiothoracic critical care unit. Interest in this region
is limited largely to distension and the presence of
bowel sounds or the absence thereof. However, small The Unconscious Patient
or large bowel ischaemia is a not uncommon phenom- As for history, the physical examination of the uncon-
enon following cardiac surgery, as a result of a low scious individual is hindered by the lack of patient
cardiac output state, embolic phenomenon or use of participation. Nevertheless, such an examination
intra-aortic balloon counterpulsation. A high index of should always be undertaken with the same care as
suspicion is required for this condition, particularly in if the patient were awake and fully conscious. The
the setting of an unexplained lactataemia and wors- presence of the mechanical ventilator at the bedside
ening acidosis, despite the presence of a seemingly increases the ambient noise level, further impairing
adequate cardiac output. The opportunity should be the ability of the clinician to auscultate. Heavy sed-
taken at this point to assess the back of the patient for ation or neuromuscular blockade naturally prevents
sacral oedema, as this is the most dependent point in patient movement, and simple tasks such as leaning
the semirecumbent patient, and is an important find- the patient forward to auscultate the chest are impos-
ing when assessing volume status. sible. Nevertheless, an attempt should be made, as
much valuable information can still be gained, par-
The Legs ticularly with respect to tissue perfusion.
An assessment of the legs completes the examination. As for physical examination in the conscious
Like the hands, the lower extremities reveal much patient, assessment of the unconscious patient should
about perfusion status, thus capillary refill and skin follow in the same stepwise fashion. Many of the same
temperature should be assessed. The posterior tibial clinical features may be found on careful inspection.
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6
Caution should be taken during joint manipulation and examination. Whilst cardiothoracic critical care
and palpation. The patient will not be able to report requires a different skill set to that of the emergency
discomfort or resist painful movements, and tissue department or ward, the temptation to forgo the basic
damage may result if the examiner is overly rough. diagnostic process must be resisted, as history and
Examination of the abdomen in the unconscious examination findings serve to clarify the clinical scen-
patient is considerably confounded, especially in the ario and highlight evolving problems that monitoring
setting of neuromuscular blockade. This is because the may not detect for some time. Furthermore, history
early features of gut ischaemia or peritonism will be and physical examination allow appropriate targeting
absent, partly because the patient is unable to report of investigations, minimising patient discomfort and
discomfort, but also because of a lack of abdominal unnecessary cost to the health system.
muscle tone. As a result, the early features of guard-
ing and tenderness to percussion (formerly tested as Learning Points
‘rebound tenderness’) are absent. Consequently,
• The cardiothoracic intensivist should adopt an
abdominal distension, free gas under the diaphragm
inquisitive approach to history and physical
and a rising lactate in the setting of apparently
examination so as to confirm previous findings,
adequate cardiac output may be the only features of
assess disease progression and exclude new
a major intra-abdominal pathology. A high index of
pathology.
suspicion must be maintained as a result.
Daily assessment of the unconscious patient • It can be challenging to elicit a history and
should also include a brief neurological examination. undertake a physical examination in the critically
Naturally, a full assessment of muscle power cannot ill patient and it may be necessary to modify the
be undertaken, but a brief examination for features of conventional stepwise approach.
an upper motor neurone lesion such as hypertonia, • Advanced monitoring modalities are prone to
hyperreflexia and clonus (in the absence of neuromus- artefact and incorrect interpretation and should
cular blockade) can be quickly and easily performed. not be seen as a substitute for a thorough history
As described in detail in Chapter 16, on sedation and physical examination.
and analgesia, the indications for deep sedation and • On admission/discharge from cardiothoracic
neuromuscular blockade are becoming fewer as car- critical care a formal handover of clinical
diothoracic critical care evolves, and targeted sed- information is an absolute prerequisite for
ation and sedation breaks are increasingly de rigueur. continuity of care.
Conscious state can be graded with any number of • It may be necessary to explore and document
specialist sedation scores, which are beyond the scope a patient’s specific wishes in a number of
of this chapter –however, response to approach, hypothetical clinical scenarios so as to inform
voice and pain should be assessed. A variety of dif- decision making should the patient deteriorate.
ferent techniques have been described to evaluate
response to painful stimulus. However, firm pressure Further Reading
over the superior orbital notch is usually the most Arrowsmith JE. Symptoms and signs of cardiac
unambiguous means of assessing global response, disease. In: Mackay JH, Arrowsmith JE (Eds).
as peripheral stimulation may not give an accurate Core Topics in Cardiac Anesthesia, 2nd Edition.
assessment of localisation if a hemiplegia is present. Cambridge: Cambridge University Press, 2012,
Likewise, withdrawal to stimulation, decerebrate and pp. 75–80.
decorticate posturing can be difficult to assess when Campeau L. Grading of angina pectoris. Circulation. 1976;
the focus point is on the hand or foot. 54: 522–523.
Criteria Committee of the New York Heart Association.
Conclusions Nomenclature and Criteria for Diagnosis of Diseases
of the Heart and Great Vessels, 9th Edition. Boston,
The presence of advanced monitoring modalities and MA: Little Brown & Co, 1994, pp. 253–256.
ready access to bedside investigations, combined with Glynn M, Drake WM (Eds). Hutchison’s Clinical
difficult examination conditions, are all powerful moti- Methods: An Integrated Approach to Clinical Practice.
vators to de-emphasise the traditional focus on history Oxford: Saunders, 2012.
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7
Section 1 Diagnosis
Electrocardiography
Chapter
2 David Begley
Introduction Precordial (Chest) Electrodes

Electrocardiography (ECG) has been the main heart Most errors occur in placement of the chest electrodes,
investigation method for most of the twentieth cen- especially V1 and V2, which may be placed too high.
tury and still plays a pivotal role in diagnostics. ECGs This can have a significant effect on the resultant ECG.
can provide a wealth of information about cardiac Correct anatomical positioning must be adhered to,
function and can often show early signs of systemic with the centre of the electrode aligned with the cor-
abnormalities as well. In order to accurately inter- rect location.
pret an ECG it is important to first ensure its correct • V1 (C1) fourth intercostal space, right sternal
acquisition. The process involves recording small edge
electrical changes on the skin that occur as a result • V2 (C2) fourth intercostal space, left sternal
of cardiac muscle depolarisation. Ten electrodes are edge
used to record the heart’s electrical activity in 12 dif-
• V3 (C3) midway between V2 and V4
ferent orientations, which encompass the 12 ‘leads’ of
• V4 (C4) fifth intercostal space, midclavicular
the ECG. It is important therefore to ensure that these
line
10 electrodes are consistently applied in order to
accurately assess for any abnormalities. In addition, • V5 (C5) horizontal level with V4, anterior
account must be made of sources of interference. axillary line
• V6 (C6) horizontal level with V4, midaxillary
line
Recording the ECG After placement of V1 and V2, V4 is located in the fifth
As posture may affect the appearance of the ECG it
intercostal space, midclavicular line. V3 is then placed
is preferably performed in the supine position where
directly in between V2 and V4. V5 and V6 are located at
practicable. Skin preparation is important to reduce
the same horizontal level as V4, perpendicular to the
artefacts and may include hair removal and/or skin
midclavicular line.
cleansing.
Limb Electrodes Filter Settings and Calibration

Most filter settings are set by default but it is recom-
Moving the limb electrodes away from the distal
mended that the low frequency filter is set on or below
limbs may affect the ECG appearance and it is there-
0.05 Hz. This filter will account for respiration. If it is
fore preferable that these are placed just proximal to
set too high, it will distort the ST segment. This may
the wrists and ankles in order to produce consistent
also reduce the accuracy of detecting myocardial
results. Limb electrodes are often colour coded to aid
ischaemia based on ST segment shifts. The high filter
placement.
setting should be set on or above 100 Hz. This filter set-
• Right arm (RA, red) proximal to right wrist ting should account for the artefact created by muscle
• Left arm (LA, yellow) proximal to left wrist tremor. The mains filter (50 Hz) is normally set to ‘Off ’.
• Left leg (LL, green) proximal to left ankle A standard ECG has a voltage calibration of
• Right leg (RL, black) proximal to right ankle 10 mm/mV and is recorded with a paper speed of
13:37:33 7
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8
25 mm/s. This results in 10 second recording. Each –90°

small square is equal to 40 ms and each large square (5
small squares) is equal to 200 ms.
The 12 ‘Lead’ ECG
aVR –150° aVL –30°
The 12 ‘leads’ of an ECG correspond to 12 vec-
tors along which depolarisation of cardiac tissue is
recorded. Each is created by measuring the electrical
potential between two points. In each case one of the
±180° I 0°
ten electrodes is the positive pole. There are three
bipolar limb leads where another electrode is the
negative pole. The negative pole for the unipolar limb
leads and the precordial leads is a composite pole
(VW) called Wilson’s central terminus, which is cre-
ated by averaging the potential recorded by RA, LA
and LL electrodes: III +120° II +60°
VW = 1/3 (RA + LA + LL). aVF +90°
The six limb leads view the heart in the coronal (ver- Figure 2.1 Hexaxial reference system.
tical) plane while the six precordial leads view the
heart in a perpendicular transverse (horizontal) plane. The vectors created by the bipolar and augmented limb
leads together form the hexaxial reference system (see
Bipolar Limb Leads Figure 2.1).
• Lead I is the potential difference between
LA and RA, Precordial Leads
I = LA – RA. For each of the precordial leads the positive pole
is the corresponding electrode and the negative pole
• Lead II is the potential difference between
is VW.
LL and RA,
II = LL – RA.
ECG Arrangement
• Lead III is the potential difference between A standard ECG records a 2.5 second tracing of each
LL and LA, lead arranged in a grid of four columns and three
III = LL – LA. rows. A marker depicts the change from one lead to
the next in each row and can be confused with part
Unipolar Augmented Limb Leads of the ECG. The first column contains leads I, II and
III, the second column aVR, aVL and aVF, the third
• Lead aVR is the potential difference between column V1, V2 and V3 and the final column contains
RA and Vw, leads V4, V5 and V6. A fourth row is often provided as
aVR = 3/2 (RA – VW). a continuous tracing to aid determination of rhythm.
• Lead aVL is the potential difference between Although each lead records electrical activity of
LA and Vw , the heart from a different angle, contiguous leads are
associated with different anatomical regions.
aVL = 3/2 (LA – VW).
• Inferior leads II, III and aVF
• Lead aVF is the potential difference between • V3 and V4
Anterior leads
LL and Vw , • Septal leads
V1 and V2
aVF = 3/2 (LL – VW). • Lateral leads I, aVL, V5 and V6
13:37:33
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9
Chapter 2: Electrocardiography
Interpretation of the ECG of which are perfect. Most commonly used is the

Sokolow–Lyon index:
Waves and Intervals • S wave in V1 + R wave in V5 or V6 (whichever
largest) > 3.5 mV.
P Wave
There is a large S wave in lead V1, which gradually
The P wave (see Figure 2.2) represents depolarisation becomes smaller (absent) by lead V6. Its presence or
of the right and left atria. In normal sinus rhythm, its absence is rarely of clinical significance.
origins are from the sinus node, which is normally
located posteriorly high in the right atrium. Therefore, J Point
the P wave is positive (upright) in all leads except aVR, The J point is the junction between the QRS complex
and can be positive or biphasic in V1. It typically has and the subsequent ST segment. Elevation or abnor-
duration <80 ms. malities of the J point are frequently seen and their
In right atrial enlargement, the P wave is tall significance is debated. Elevation of the J point is
and peaked, and is prolonged and bifid in left atrial observed in hypothermia.
enlargement.
ST Segment
PR Interval The ST segment is the section between the end of the
The PR interval is measured from the beginning of QRS complex (J point) and the T wave. It is typically
the P wave to the beginning of the QRS complex and isoelectric and represents the period of time when the
represents the time taken for atrial depolarisation ventricles remain depolarised prior to repolarisation. If
and conduction through the AV node. A normal PR the ST segment is down sloping or depressed, this may
interval varies between 120 and 200 ms. indicate myocardial ischaemia. ST segment elevation,
If the PR interval is shorter than 120 ms then taken as more than 1 mm, 80 ms following the J point,
conduction is bypassing the AV node (see Wolf– may indicate myocardial infarction but has a false posi-
Parkinson–White syndrome). Prolongation of the PR tive rate between 15 and 20% (even slightly higher in
interval indicates 1° AV block. Depression of the short women). Abnormalities of the ST segment can also
isoelectric segment between the end of the P wave occur in pericarditis and left ventricular hypertrophy.
and the beginning of the QRS complex can indicate
pericarditis. T Wave
The T wave represents ventricular repolarisation. It
QRS Complex is typically positive in all leads except aVR and V1.
Q, R and S waves form the QRS complex, which rep- A variety of situations can result in T wave abnor-
resents ventricular depolarisation. If the first deflec- malities, which are often non- specific. Myocardial
tion is negative it is termed the Q wave, otherwise an ischaemia and left ventricular hypertrophy can result
initial positive deflection is an R wave. A final nega- in T wave inversion. Metabolic abnormalities can also
tive deflection is the S wave. Normally the whole QRS manifest as T wave abnormalities.
complex is <120 ms in duration. Q waves represent
left to right depolarisation of the interventricular U Wave
septum and are typically seen in left sided leads (I, The U wave is poorly understood but may represent
aVL, V5 and V6). Small Q waves can be seen in most repolarisation of the interventricular septum or pap-
leads except V1, V2 and V3. illary muscles and therefore can be observed on the
Large Q waves are pathological if >40 ms wide, normal ECG, although their absence is not patho-
and >2 mm deep or >25% of the height of the QRS logical. Prominent U waves are observed in hypokal-
complex. This can represent myocardial infarction, aemia and hypothyroidism.
cardiomyopathy or electrode malposition.
If the QRS complex is particularly tall this may QT Interval
indicate left ventricular hypertrophy. A number of The QT interval is measured from the beginning of
criteria have been developed to aid diagnosis, none the QRS complex to the end of the T wave. There are
13:37:33 9
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10
-QRS Width-
ST
-PR Interval- - -
Segment
T
P
-QT Interval-
Figure 2.2 PQRST intervals.
several issues regarding its measurement, not least the result of a genetic abnormality or due to a variety
determining where the T wave ends. The best lead of medications.
to measure the QT interval is lead V3 or II. Several
consecutive beats should be measured with the long-
est value taken. Prominent U waves are not normally
Rate and Rhythm
included in the calculation and the end of the T wave Heart Rate
is then assumed to be where the downslope of the T The heart rate is most accurately obtained by dividing
wave would cross the isoelectric line. If depolarisation the cycle length (RR interval) into 60,000. However,
is prolonged, the difference between the measured this is more easily achieved by dividing the number
QRS complex and 120 ms should be subtracted from of large squares on a standard ECG between succes-
the measured QT interval. sive QRS complexes into 300. These formulae work
Because of the close relationship of the QT interval well provided the rhythm is regular. However, if the
and heart rate (the QT shortens with increasing heart rhythm is irregular then we can take advantage of
rate), a correction factor must be applied. Although the fact that the ECG is recorded over 10 seconds.
many methods have been developed to calculate a cor- Counting the number of QRS complexes across the
rected QT (QTc), the one most widely used is Bazett’s ECG and multiplying by 6 will give an estimate of the
formula: heart rate.
QTc = QT / √RR interval.
Rhythm
The RR interval is measured in seconds such that at a The presence of P waves on their own does not indi-
heart rate of 60 bpm the RR interval is 1, and QTc = QT. cate sinus rhythm. It is important to ensure that their
The QTc is typically less than 440 ms. Gender, how- morphology (as discussed earlier) is consistent with an
ever, also has an effect on QTc and therefore a value of origin from the sinus node. A disparate morphology
less than 460 ms is acceptable for women. might indicate an ectopic atrial origin and prompt
An abnormally prolonged QTc can predispose to closer scrutiny. If the P wave is not clear on the surface
malignant ventricular arrhythmias. A long QT can be ECG then, post cardiac surgery, the temporary atrial
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11
Lead I +ve
Lead II –ve
aVL Left Axis aVL

aVR aVR
Deviation
Lead I +ve
I I
Normal
Axis
III II III II
aVF aVF
Lead II +ve
Lead II –ve
(aVF –ve)
Lead I –ve
aVR aVL aVR Indeterminate aVL

Axis
I I
Right Axis
Deviation
Lead I –ve
III II III II
aVF Lead II +ve aVF
(aVF +ve)
Figure 2.3 Mean frontal axis.
pacemaker wires can be used to create an atrial elec- block). A normal QRS axis is usually between −30°
trocardiogram (AEG). This is recorded by connect- and +90°.
ing the atrial pacing wires to the left and right arm The mean frontal axis provides a mean electrical
leads, or to one of the precordial chest leads, and may ventricular depolarisation vector in two dimensions
be useful in differentiating various tachy and brady only. The QRS transition provides an indication of the
arrhythmias. ventricular depolarisation in the third dimension (z
axis). The QRS transition is determined from the pre-
Axis and QRS Transition cordial leads. The QRS complex in lead V1 is usually
negative and gradually becomes more positive through
The mean frontal axis (Figure 2.3) of the heart pro-
V6. The transition zone is where the QRS changes from
vides an average electrical axis (vector) of ventricular
being predominantly negative to being predominantly
depolarisation. Any deviation from a normal axis may
positive. This usually occurs at V3 or V4.
indicate pathology. This may be in the form of struc-
tural abnormalities (i.e. increased muscle mass –left
ventricular hypertrophy or loss of muscle mass –fol- Calculating the QRS Axis
lowing myocardial infarction) or electrical abnormal- To estimate the QRS axis we focus solely on the limb
ities (i.e. accessory AV connections or bundle branch leads (not V1–V6) and use the fact that depolarisation
13:37:33 11
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12
towards any lead will provide a positive deflection in left anterior fascicle results in left axis deviation and
that lead. less marked widening of the QRS complex. This is
If lead I is positive, the axis must lie between −90° called left anterior hemiblock (LAHB). A qR com-
and +90°. If lead II is negative, then the axis is between plex is observed in lateral leads I and aVL, and rS
−30° and −240°. Together the axis must be between pattern in the inferior leads II, III and aVF. Due to
−30° and −90°. This is left axis deviation. its broad nature and dual blood supply, left posterior
If lead I is negative, the axis must lie between hemiblock (LPHB) is much less common. It is charac-
−90° and −270°. If lead aVF is positive, the axis must terised by right axis deviation, a rS complex in lateral
be between 0° and 180°. Together the axis must be leads and qR complex in inferior leads.
between −90° and 180°. This is right axis deviation.
If lead I is negative and lead aVF is negative, AV Block
then the axis lies between −90° and 180°. This is an When conduction between the atria and ventricles
indeterminate axis. is impaired, AV block is said to be present. If the PR
interval is prolonged beyond 200 ms but each P wave
Arrhythmias remains associated with a single QRS complex, 1° AV
block is present.
Conduction Abnormalities Progressive beat-to-beat prolongation of the PR
interval with the final beat not conducting to the
Bundle Branch Block ventricles is Mobitz 1 2° AV block (Wenckebach
Electrical impulses transmitted through the AV node phenomenon). However, if the PR interval remains
and bundle of His are conducted to the ventricular unchanged prior to loss of conduction to the ventri-
myocytes via the left and right bundles. cles then Mobitz 2 2° AV block is present.
The right bundle remains sheathed in connective When there is complete dissociation between
tissue within the septum until it reaches the base of the atrial and ventricular depolarisation (i.e. no associ-
papillary muscle when it divides into multiple fibres ation between P waves and QRS complexes) 3° AV
connecting with the Purkinje fibres. The left bundle block is present.
however divides immediately into anterior and pos-
terior fascicles supplying Purkinje fibres within the Tachyarrhythmias
left ventricle.
Supraventricular Arrhythmias
Right bundle branch block (RBBB) occurs when Atrial flutter: Atrial flutter refers to any macro re-
there is loss of conduction through the right bundle entrant rhythm within the atria. Typical atrial flutter
branch. The left ventricle is excited normally by the is a right atrial rhythm where depolarisation occurs
left bundle branch but the right ventricle is depolar- continuously, usually in a counterclockwise fashion,
ised via conduction through the myocardium from around the tricuspid valve. The AV node will conduct
the left ventricle. As a result, ventricular depolarisa- at a variable rate depending on other factors such as
tion is prolonged and there is an extra deflection indi- concomitant medication etc. The resultant ECG dem-
cated by rapid left ventricular depolarisation followed onstrates a continuously cycling baseline between QRS
by slower right ventricular depolarisation. A QRS dur- complexes. These ‘flutter’ waves have a slow phase and
ation >100 ms indicates incomplete block and a dur- a fast phase, are negative in the inferior leads, positive
ation >120 ms indicates complete block. A terminal in lead V1 and isoelectric in lead I which is perpen-
R wave is observed in lead V1 (rsRʹ) and a slurred S dicular to the re-entrant circuit.
wave in leads I and V6. The T wave should be deflected
opposite the terminal deflection of the QRS complex. Atrial fibrillation (AF): Although theories regarding
Right bundle branch block can be observed in normal the exact mechanisms responsible for atrial fibrilla-
individuals without cardiac disease. tion abound, it is still poorly understood. In essence,
however, there are multiple re-entrant circuits and
Left bundle branch block (LBBB) is demonstrated by wavelets that are constantly colliding and interrupt-
a QRS >120 ms, a QS or rS complex in lead V1 and a ing each other. The AV node is continuously receiving
notched R wave in lead V6. Involvement of only the impulse, which again will be conducted at a variable
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13
rate. The ECG will demonstrate a chaotic baseline, be assessed and treated promptly within current
constantly changing in frequency and amplitude. guidelines. Distinguishing between ventricular
tachycardia and supraventricular tachycardia with
AV node re-entrant tachycardia (AVNRT): The AV aberrant ventricular depolarisation can be difficult.
node receives multiple inputs within the transition Clearly dissociated P waves, fusion beats (partial ven-
zone around the compact AV node. These inputs may tricular depolarisation over the AV node) and cap-
have different properties with regards to conduction ture beats (complete ventricular depolarisation over
velocities and refractory periods. This discordance the AV node) are all good indicators of VT but are
can result in a re-entrant rhythm between the different frequently absent. Other features, which are sug-
connections. The ECG depicts a regular narrow com- gestive of VT are:
plex tachycardia with no discernable P waves as both
atria and ventricles are depolarised simultaneously. • Absence of typical LBBB or RBBB
• Indeterminate axis
AV re- entrant tachycardia (AVRT): Additional • Very broad QRS >160 ms
accessory electrical connections between the atria • Positive/negative concordance
and ventricles can result in pre-excitation. The rela- • R wave > Rʹ in V1.
tively quick conduction over the accessory connec-
tion results in the ventricle beginning to depolarise
from an area other than those directly supplied by
Learning Points
the bundle branches. This ventricular depolarisation • Accurate electrode placement is essential to ECG
is fused with depolarisation from the normal conduc- interpretation.
tion system as signals catch up through the AV node. • Care should be taken to examine all leads when
The slurred onset of the resultant QRS complex is making measurements.
termed a ‘delta’ wave and represents pre-excitation. • QRS axis and transition can be used together
Under certain circumstances, impulse can con- to indicate underlying ventricular
tinuously cycle between the AV node and accessory abnormalities.
connection. If the AV node is the anterograde limb of • Narrow complex tachycardias can often be
the circuit, the resultant arrhythmia is orthodromic distinguished by their ECG features.
AVRT. Rarely, the accessory connection is the antero- • Broad complex tachycardias should be considered
grade limb and the resultant arrhythmia is antidromic to be ventricular tachycardia until proved
AVRT. The ECG of orthodromic AVRT will show a otherwise.
narrow complex tachycardia (no pre-excitation evi-
dent) with inverted P wave discernible shortly after Further Reading
the QRS complex. Antidromic AVRT will show a
Bazett HC. An analysis of the time-relations of
maximally pre-excited QRS complex. electrocardiograms. Heart. 1920; 7: 353–370.
Subjects with pre-excitation and symptoms that
Eldridge J, Richley D. Recording a standard 12-lead
may be related to it (palpitations, breathlessness, electrocardiogram. An Approved Methodology by
presyncope and syncope) are said to have Wolff– the Society for Cardiological Science & Technology
Parkinson–White syndrome (WPW). (SCST), 2014.
Sokolow M, Lyon TP. The ventricular complex in left
Ventricular Arrhythmias ventricular hypertrophy as obtained by unipolar
A broad complex tachycardia is ventricular tachy- precordial and limb leads. American Heart Journal.
cardia (VT) until proved otherwise. Patients should 1949; 37: 161–186.
MCQs
1. Electrode V2 is positioned at the following position: (c) Left sternal edge, 3rd intercostal space
(a) Right sternal edge, 3rd intercostal space (d) Left sternal edge, 4th intercostal space
(b) Right sternal edge, 4th intercostal space (e) Left sternal edge, 5th intercostal space
13:37:33 13
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14
2. The QTc attempts to correct the QT interval to a heart 4. A gradual beat-to-beat lengthening of the PR interval
rate of: followed by a dropped beat is known as:
(a) 50 (a) 1° AV block
(b) 55 (b) Mobitz 1 2° AV block
(c) 60 (c) Mobitz 2 2° AV block
(d) 70 (d) Complete AV block
(e) 75 (e) Normal
3. A normal QRS axis lies between: 5. An ECG with a continuously cycling regular baseline
(a) −90° and +90° between QRS complexes is likely to be showing:
(b) −30° and +90° (a) Atrial flutter
(c) −30° and +120° (b) Atrial fibrillation
(d) 0° and +90° (c) AVNRT
(e) 0° and +120° (d) Orthodromic AVRT

(e) Antidromic AVRT
Exercise answers are available on p.467. Alternatively, take the test online at www.cambridge.org/CardiothoracicMCQ
13:37:33
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15
Section 1 Diagnosis
Echocardiography in the Cardiothoracic

Chapter
3 Intensive Care Unit
Ghislaine Douflé and Andrew Roscoe
Introduction PLAX PSAX

Since its introduction into the intensive care environ-
ment in the early 1980s, echocardiography has been
recognised as an invaluable tool. Transthoracic echo-
cardiography (TTE) provides a non-invasive, portable
imaging modality, which allows for rapid diagnosis
and cardiovascular monitoring in the critically ill.
Transoesophageal echocardiography (TOE) produces
A4C SC
better resolution images and is often utilised as an
adjunct, or when TTE image quality is inadequate.
Focused echocardiography provides a goal
directed ultrasound examination to address specific
diagnostic and monitoring questions.
Indications for Echocardiography

Figure 3.1 Basic focused transthoracic echocardiography views.
In the critically ill patient echocardiography has been PLAX, parasternal long-axis; PSAX, parasternal short-axis; A4C, apical
shown to provide supplemental information to phys- four-chamber; SC, subcostal.
ical examination and other monitoring modalities. It
may be performed for diagnostic reasons, as a haemo-
dynamic monitor, to assess volaemic status, or for development of skills to obtain adequate ultrasound
procedural guidance. images, but also the knowledge to interpret the find-
ings and the experience to request a comprehensive
Focused Scanning study when indicated. Consequently, training and
accreditation programmes are now established to
A focused TTE evaluation comprises four views of the
ensure competency and focused echo is a skill to be
heart: parasternal long-axis and short-axis, apical four-
possessed by all critical care physicians.
chamber and subcostal views (Figure 3.1). Each view
provides basic information on biventricular function,
volaemic status, valvular function, and the presence Left Ventricle
of pleural or pericardial collections. When integrated Left ventricular (LV) systolic function (LVSF) is fre-
with clinical examination and other haemodynamic quently altered in the critically ill, either as a cause
parameters, point-of-care echocardiography provides of decompensation, or as a consequence of critical
a bedside tool for diagnosis and monitoring of cardio- illness: the incidence of LVSF in septic shock, for
vascular pathophysiology. Multiple focused cardiac example, may be as high as 60%.
scanning protocols are now in use across the globe Advances in perioperative management and myo-
(e.g. FICE, FEEL, FATE) and extended algorithms cardial protection have seen a reduction in the inci-
have been developed to allow basic assessment of dence of postcardiotomy cardiogenic shock, but it
valvular pathology and quantification of ventricular may still occur in up to 6% of cardiac surgical pro-
function. Focused scanning requires not only the cedures, and is associated with high mortality. Early
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Figure 3.2 TOE midoesophageal four-chamber (a) and two-chamber (b) views, showing biplane method (modified Simpson’s rule) to
derive left ventricular ejection fraction.
postoperative detection or exclusion of LV dysfunc- The modified Simpson rule involves tracing the LV
tion is paramount to initiate prompt and appropriate cavity in the four-chamber and two-chamber views
therapy. at end-diastole and end-systole to estimate LVEDV
Although some studies have reported good correl- and LVESV (Figure 3.2). Three-dimensional echocar-
ation between qualitative and quantitative assessment, diography has also been shown to produce accurate
objective quantification of LVSF is recommended and and reproducible measures of LV volumes. EF is
allows for interobserver comparisons. calculated as:
Fractional shortening (FS), derived from M-mode
linear measurements, is a quick and reproducible EF = (LVEDV – LVESV) / LVEDV.
measure of LVSF. However, it is only representative
of a single dimension, and in the presence of regional The presence of RWMA before and after cardiac
wall motion abnormalities (RWMA) may give an surgery is not uncommon, but the detection of new
inaccurate measure of global LVSF. defects warrants further investigation. After coronary
Ejection fraction (EF) is calculated from estimates artery bypass grafting (CABG) surgery, a new RWMA
of LV end-diastolic volume (LVEDV) and end-systolic suggests myocardial ischaemia or possibly infarction
volume (LVESV). EF derived from the FS, using the from multiple causes including a compromised cor-
Teichholz method, is limited by its assumptions of the onary artery bypass graft occlusion, coronary vaso-
geometric LV shape, and is no longer recommended. spasm, inadvertent left circumflex artery ligation
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Chapter 3: Echocardiography
during mitral valve (MV) surgery (presenting with In the presence of tricuspid regurgitation (TR), RV
LV lateral wall akinesia), coronary ostial compromise systolic pressure can be reliably estimated by applying
after aortic root surgery and others. The 17-segment the simplified Bernoulli equation to the peak TR jet
LV model is typically used and each segment is scored velocity.
as follows: Due to its geometry, echocardiographic quan-
1 normokinesia, normal regional wall motion tification of RV systolic function is challenging.
2 hypokinesia, reduced regional wall motion Longitudinal measures of function, such as tricuspid
3 akinesia, no movement of one or more annular plane systolic excursion (TAPSE) and tissue
segments Doppler derived tricuspid lateral annular systolic vel-
4 dyskinesia, paradoxical movement of one or more ocity (Sʹ), provide excellent measures of RV function.
segments in relation to other LV areas. They are easily obtainable by TTE, but with TOE,
values can be underestimated due to linear malalign-
However, RWMA may occur in the absence of sig-
ment. Their use in the perioperative setting is less
nificant coronary artery disease: postoperative epi-
robust: opening of the pericardium is accompanied
cardial pacing induces abnormal motion of the
by a significant decline in TAPSE and Sʹ without
interventricular septum (IVS) and posterior LV;
an associated decrease in global RV function. This
stress induced (Takotsubo) cardiomyopathy clas-
makes preoperative and early postoperative com-
sically presents with apical akinesia and ballooning;
parisons unreliable. RV fractional area change (FAC)
the inferior and inferolateral LV walls are most often
provides an accurate measure of global RV function
affected in myocarditis.
(Figure 3.3), correlates with RVEF derived from mag-
The assessment of LV diastolic function should
netic resonance imaging and is an independent pre-
form an integral part of a routine examination, espe-
dictor of mortality. Global longitudinal strain and
cially in patients presenting with heart failure. In fact,
three-dimensional imaging offer alternative measures
up to 50% of patients with CHF have isolated LV dia-
of RV performance.
stolic dysfunction (DD) in the presence of a normal
LVEF. In addition, LVDD may play an important role
in a subset of patients difficult to wean from mechan- Valvular Heart Disease
ical ventilation. In the early postoperative period, echocardiography is
Patients with dynamic LV outflow tract (LVOT) used to assess adequacy of valve repair, competence of
obstruction exhibit hypotension, a low cardiac index valve replacement, detection of significant paravalvu-
and high LV filling pressures, but deteriorate with ino- lar leaks, recognition of patient-prosthesis mismatch,
tropic administration. Typically seen in hypertrophic and iatrogenic valve injury.
obstructive cardiomyopathy (HOCM) and post-MV Valvulopathies responsible for acute deterior-
repair surgery, it may also occur in severe hypovol- ation can be postischaemic, infective and traumatic in
aemia. Echocardiography is indispensable in making origin. Acute myocardial infarction (MI) may be com-
the correct diagnosis, allowing expeditious treatment plicated by papillary muscle rupture and severe MR.
revision to vasopressor therapy, volume loading and Infective endocarditis (IE) is a life threatening condi-
cessation of inotropic support. Echocardiography tion. TOE is recommended in patients with high clin-
findings include the presence of a significant gradient ical suspicion of IE. It is essential to determine the size
in the LVOT, systolic anterior motion (SAM) of the and precise location of vegetations, extent of leaflet
MV and mitral regurgitation (MR). destruction and valvular dysfunction, the presence
of abscess cavities or fistulae, and dehiscence of pros-
Right Ventricle thetic valves (Figure 3.4). Echocardiography findings
are crucial in predicting embolic risk and establishing
Acute right ventricular (RV) failure after cardiac sur-
the timing of surgical intervention.
gery carries a poor prognosis. It occurs frequently after
heart transplantation and LV assist device (LVAD)
implantation. RV dysfunction is a well- recognised Pericardium
complication of acute respiratory distress syndrome Cardiac tamponade is a clinical diagnosis comprising
(ARDS) and RV-protective ventilation strategies have haemodynamic instability associated with equalisa-
emerged to impact on RV function. tion of diastolic filling pressures and large respiratory
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Figure 3.3 TOE midoesophageal four-chamber right ventricular views in end-diastole (a) and end-systole (b), used to calculate right
ventricular fractional area change.
Figure 3.4 TOE midoesophageal long axis view, showing Figure 3.5 TTE subcostal view, showing a large pericardial
vegetations (arrows) on the aortic valve (AV). LA, left atrium; LV, left effusion (arrows). LV, left ventricle; RV, right ventricle.
ventricle.
patients, echocardiography may be utilised to monitor

fluctuation in arterial pressure (pulsus paradoxus). the progression of a pericardial effusion.
After cardiac surgery, however, classic signs of cardiac Constrictive pericarditis (CP) results in impaired
tamponade are often mild and atypical presentations diastolic filling due to a rigid, non-compliant peri-
are not uncommon. Localised pericardial collections cardium. Patients present with chest pain, dyspnoea
and thrombus formation may cause isolated left-sided and peripheral oedema. Although usually idiopathic
compression, with normal right- sided pressures. in origin, it can occur post-MI and postcardiac sur-
A high index of suspicion is required postcardiac gery. It is important to differentiate it from restrictive
surgery and TTE or TOE often provides rapid con- cardiomyopathy (RCM).
firmation of diagnosis (Figure 3.5). Loculated and Echocardiographic features to distinguish CP from
posterior collections may necessitate TOE. In patients RCM include a hyperechogenic pericardium, dynamic
with significant pulmonary hypertension, RV diastolic changes in LV diastolic filling velocity with respiration
collapse may be absent. In haemodynamically stable and preservation of myocardial relaxation velocities.
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19
Aorta
Aortic dissection typically presents with chest pain
and symptomology overlaps that of acute MI, how-
ever, it may be asymptomatic perioperatively. Contrast
computed tomography (CT) and cardiac magnetic
resonance (CMR) usually confirms the diagnosis,
but TOE may assist in demonstrating complications,
including aortic regurgitation (AR), pericardial effu-
sion, pleural effusion and RWMA secondary to cor-
onary involvement of the dissection flap. In particular,
TOE examination of the mechanism of AR is essential
to determine the surgical plan.
In the haemodynamically unstable postoperative
patient, an echocardiographic study must include Figure 3.6 TOE midoesophageal bicaval view, showing thrombus
assessment of the aorta: the incidence of intraoperative (arrows) attached to a central venous catheter (CVC), in the right
iatrogenic type A dissection is approximately 0.2%. atrium (RA). LA, left atrium; SVC, superior vena cava.
Intracardiac Shunts (McConnell’s sign), peak TR jet velocity >2.7 m/s and

Previously undiagnosed interatrial shunts may pre- pulmonary artery acceleration time <80 ms all sup-
sent with hypoxaemia or paradoxical emboli, particu- port the diagnosis of PE.
larly in patients subjected to increased positive airway
pressures. Right-to-left shunting via a persistent for- Cardiac Arrest
amen ovale is observed in up to 20% of patients with A focused TTE exam may be of value in the rapid
ARDS and refractory hypoxaemia. identification of reversible causes of cardiac arrest. To
Post-MI cardiogenic shock may be precipitated by avoid interruptions in chest compressions, a subcostal
ventricular septal defect that often requires placement view is obtained during the 10-second pulse check.
of an intra-aortic balloon pump and urgent surgical Readily detectable reversible causes include hypovol-
correction. Echocardiographic examination must aemia, tamponade, tension pneumothorax, myocar-
exclude this rare but life threatening complication in dial ischaemia and signs of PE.
patients with haemodynamic instability after an MI
involving the interventricular septum.
Trauma
Chest wall trauma usually precludes the acquisi-
Intracardiac Masses tion of adequate TTE views. TOE, as the preferred
Cardioembolism accounts for 15–30% of ischaemic modality, aids in the diagnosis of myocardial con-
strokes. Echocardiography represents the mainstay tusion, pericardial effusion, and valvular and aortic
in evaluation for left-sided cardiac masses. In atrial injuries.
fibrillation, thrombus typically develops in the left
atrial appendage; thrombus also occurs in areas of
LV akinaesia or aneurysm, and on pacemaker wires
Haemodynamic Monitoring
Inferior vena cava (IVC) diameter and its respira-
or indwelling catheters in the right side of the heart
tory variation as a marker of fluid responsiveness has
(Figure 3.6). Other potential embolic sources include
been well characterised. Initially described in spon-
tumours and vegetations.
taneously breathing patients, its extension to the ven-
tilated population remains debatable. The effect of
Pulmonary Embolism positive pressure tidal volumes and pulmonary com-
Although CT remains the gold standard for the diag- pliance on IVC variability makes interpretation prob-
nosis of pulmonary embolism (PE), echocardiography lematic. Even with spontaneous ventilation, increased
may be of value for the patient too unstable to transfer work of breathing with the generation of extreme
to the radiology suite. RV dilatation, RV dysfunction negative intrathoracic pressures IVC collapsibility can
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20
be misleading. IVC collapsibility and distensibility • Comprehensive training is essential to ensure

indices have been developed to improve reliability in appropriate use.
determining fluid responsiveness. The superior vena • Objective quantification of ventricular function is
cava (SVC), an intrathoracic structure, offers a more recommended.
reliable parameter of fluid responsiveness in the venti- • Echocardiography has an increasing role to play
lated patient, but requires TOE for visualisation. in patients on ECLS.
LV end-diastolic area (EDA) can be easily mea
sured in short- axis views of the heart. Reduced
LVEDA is suggestive of hypovolaemia and may pre-
Further Reading
Charron C, Caille V, Jardin F, et al. Echocardiographic
dict fluid responsiveness. However, in the presence of measurement of fluid responsiveness. Current Opinion
RV failure, the LV will appear underfilled, and inspec- in Critical Care. 2006; 12: 249–254.
tion of the LV in isolation may result in inappropriate
Chockalingam A, Mehra A, Dorairajan S, Dellsperger KC.
fluid administration. Measurement of LVOT velocity- Acute left ventricular dysfunction in the critically ill.
time integral (VTI) provides a surrogate for LV stroke Chest. 2010; 138: 198–207.
volume. Respiratory variation in LVOT VTI has been Doufle G, Roscoe A, Billia F, et al. Echocardiography
used to guide fluid responsiveness and to calculate the for adult patients supported with extracorporeal
cardiac output. membrane oxygenation. Critical Care. 2015;
19: 326.
Procedural Guidance Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/AHA/
ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011
Ultrasound plays a pivotal role in the field of mech-
Appropriate use criteria for echocardiography. Journal
anical circulatory support. Intra-aortic balloon pump of the American Society of Echocardiography. 2011;
insertion and positioning can be optimised by TOE, 24: 229–267.
and immediate aortic complications readily detected. Expert Round Table on Echocardiography in ICU.
Echocardiography can be used to guide cannulation International consensus statement on training
of extracorporeal life support (ECLS), to manage standards for advanced critical care echocardiography.
patients on ECLS and to assess suitability for wean- Intensive Care Medicine. 2014; 40: 654–666.
ing from support. Pericardiocentesis should be per- Krishnan S, Schmidt GA. Acute right ventricular
formed under echocardiography guidance. dysfunction: real-time management with
echocardiography. Chest. 2015; 147: 835–846.
Summary Lang RM, Badano LP, Mor-Avi V, et al. Recommendations
for cardiac chamber quantification by
The role of echocardiography in the critical care echocardiography in adults: an update from the
setting is expanding. As with any monitoring tool, American Society of Echocardiography and the
physicians need to be aware of its limitations and European Association of Cardiovascular Imaging.
integrate the findings with the clinical context. Journal of the American Society of Echocardiography.
Comprehensive training, accreditation and mainten- 2015; 28: 1–39.
ance of skills are essential to ensure appropriate use Vignon P. Ventricular diastolic abnormalities in the
and interpretation. critically ill. Current Opinion in Critical Care. 2013;
19: 242–249.
Learning Points Walley PE, Walley KR, Goodgame B, et al. A practical
approach to goal-directed echocardiography in the
• Echocardiography is pivotal in the evaluation of critical care setting. Critical Care. 2014; 18: 681.
the unstable patient. Zafiropoulos A, Asrress K, Redwood S, et al. Critical care
• Focused echo is a skill to be possessed by all echo rounds: Echo in cardiac arrest. Echo Research
critical care physicians. Practice. 2014; 1: D15–D21.
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MCQs
True or False (c) Left ventricular outflow tract (LVOT) VTI variation
1. Regarding left ventricular systolic dysfunction: can be used to guide fluid administration
(a) The incidence in septic shock is up to 60% (d) Left ventricular end-diastolic area (LVEDA) is
measured in the long-axis views of the heart
(b) Occurs in 20% of patients after cardiac surgery
(e) Reduced LVEDA is suggestive of hypovolaemia
(c) Can be accurately quantified by fractional short-
ening in patients with regional wall motion 4. Features of left ventricular outflow tract (LVOT)
abnormalities obstruction include:
(d) Can be accurately quantified by modified Simpson’s (a) Systolic anterior motion of the anterior mitral valve
biplane method in patients with regional wall leaflet
motion abnormalities (b) Pressure gradient in the LVOT
(e) Septal wall akinesia after mitral valve surgery sug- (c) Worsening hypotension with adrenaline
gests injury to the left circumflex coronary artery administration
2. Tricuspid annular systolic plane excursion (TAPSE): (d) Mitral valve regurgitation
(a) Can easily be measured with transthoracic (e) Clinical improvement with administration of fluids
echocardiography and vasopressors
(b) Is a measure of the longitudinal function of the left 5. Cardiac tamponade:
ventricle
(a) Remains a clinical diagnosis
(c) A value >20 mm suggests right ventricular
(b) Can present with atypical features after cardiac
dysfunction
surgery
(d) Allows for calculation of the estimated right ven-
(c) Always presents with right ventricular diastolic
tricular systolic pressure
collapse
(e) Typically increases in value after pericardial
(d) Can be diagnosed by focused transthoracic
incision
echocardiography
3. Regarding fluid responsiveness:
(e) May be caused by a small loculated collection
(a) Inferior vena cava (IVC) collapsibility >50% always
indicates hypovolaemia
(b) Superior vena cava collapsibility index is a
more reliable parameter of fluid responsiveness
than IVC
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22
Section 1 Diagnosis
Coronary Angiography
Chapter
4 Unni Krishnan and Stephen P Hoole
Definition acute coronary syndromes including STEMI, heart

failure, sudden cardiac death, valvular heart disease,
Coronary angiography uses radio- opaque contrast
preoperative evaluation for non-cardiac surgery and
agent to delineate the anatomy of the coronary cir-
major organ transplantation. These are summarised
culation. This may be performed either invasively
in Table 4.1. A detailed report listing the appropriate
using specially designed intra- arterial catheters or
use criteria for coronary angiography was published
non-invasively by computerised tomography (CT)
in 2012. Appropriate use of invasive coronary angiog-
imaging. This chapter will focus on invasive coronary
raphy to investigate stable angina is also discussed in
angiography and its role in current clinical practice.
section 1.5 of the NICE guidance on the management
of stable angina.
Historical Perspective
The Nobel Laureate Werner Forssmann is credited Preprocedural Assessment
with the first cardiac catheterisation in 1929 although
this was exclusively right heart catheterisation via the Route of Arterial Access
left antecubital vein. Various reports of non-selective The latest available annual report of the British
coronary angiography in human subjects followed in Coronary Interventional Society indicates a steady
the 1940s and 1950s, culminating in the first selective increase in the use of radial access and a correspond-
(albeit serendipitous) coronary angiogram performed ing decline in femoral access for percutaneous cor-
in 1958 by Frank Mason Sones in his basement labora- onary intervention (PCI). Diagnostic angiography
tory at the Cleveland Clinic. Melvin P Judkins and has also followed a similar trend over the last decade.
Kurt Amplatz made significant modifications to the With multiple clinical trials suggesting a net reduction
technique in the 1960s. They designed catheters spe- in adverse clinical events with radial access for PCI,
cifically for selective coronary cannulation, develop- this trend is likely to continue.
ing J-tipped guidewires that were introduced via the Assessment of the peripheral arterial supply is
catheter lumen, and popularised the Seldinger tech- important before deciding the route of access for inva-
nique of percutaneous arterial access via the femoral sive coronary angiography. Symptomatic lower limb
route. Eponymously named catheters designed by peripheral arterial disease, abdominal aortic aneu-
Judkins and Amplatz are still routinely used for cor- rysms with thrombus in situ or previous vascular sur-
onary angiography today. gery (peripheral arterial bypass and/or grafts) may
preclude a femoral approach although femoral access
Indications can be gained if necessary through Gore-Tex™ grafts.
Invasive coronary angiography remains the gold Increasingly, radial arterial access is utilised, as the
standard investigation for the assessment of cor- hand has a dual arterial blood supply. Confirmation
onary anatomy. The indications for coronary angi- of ulnar artery patency (and/or radial artery patency
ography in the assessment of ischaemic heart disease in patients that have had this artery cannulated pre-
are described in detail in joint ESC, ACCF, ACC viously) is recommended by performing a modified
and AHA guidelines for the diagnosis and manage- Allen’s (or reverse Allen’s) test, plethysmography or
ment of patients with stable ischaemic heart disease, pulse oximetry.
13:40:34
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23
Chapter 4: Coronary Angiography
Table 4.1 Indications for invasive coronary angiography
Indicated Rationale
ACS (STEMI/NSTEMI/UA) High pretest probability of CAD and/or symptoms despite two antianginal
Stable CAD medications and/or a positive non-invasive function test and/or in cases
where revascularisation may improve prognosis
Prior to non-cardiac surgery
Pretransplant assessment
New diagnosis of heart failure To delineate coronary anatomy and rule out or confirm significant CAD
Survivor following sudden cardiac death/ventricular
arrhythmia
Prior to heart value surgery If age >35 years or postmenopausal at any age
Not indicated
Preoperative evaluation ‘Routine’ angiography in the absence of clinical suspicion or where
Pretransplant non-invasive tests indicate low pretest probability
Angiography of coronary artery bypass graft

conduits is traditionally performed from a fem-
Access Site Preparation
The area of skin around the access site (radial artery or
oral arterial access although the left radial artery is
femoral artery) may need to be prepared according to
also an appropriate route of access for left internal
standard aseptic surgical practice.
mammary grafts. In patients awaiting assessment
for haemodialysis, it is prudent to avoid radial access
as this is a commonly used site for arteriovenous Premedication
fistulae. An anxiolytic is useful in allaying anxiety and to avoid
spasm of the radial artery. This is usually achieved
by appropriately timed oral or parenteral benzodiaz-
History of Adverse Reaction/Allergy epines after consent has been obtained.
Any prior history of allergy to contrast agents is an
important consideration. The onset and severity of
the reaction should be explored as well as the indi-
Prehydration
cation for invasive coronary angiography before Acute kidney injury is rare following diagnostic cor-
deciding whether further contrast exposure is jus- onary angiography, which typically uses <100 ml of
tified. Although a history of seafood allergy is often contrast agent. Contrast induced nephropathy (CIN)
documented, there is no evidence to suggest that this is a form of acute kidney injury following adminis-
increases the likelihood of adverse reaction to iodi- tration of an iodinated contrast agent and is usually
nated contrast media. The risk of a serious allergic reversible. A 25% rise in serum creatinine levels from
reaction is reported as 0.02–0.5%. It is routine practice baseline at 48 hours after administration of the con-
to administer systemic steroids several hours before trast agent is often set as a threshold for diagnosis of
the procedure and antihistamines 1–2 hours prior to CIN in clinical trials. International guidelines recom-
angiography in patients with a history of suspected or mend the use of isoosmolar contrast agents to reduce
confirmed adverse reactions. the risk of CIN. Prehydration with isotonic saline has
been shown to be effective in preventing CIN espe-
cially in women, diabetics and in those requiring high
Consent volumes of contrast agent (>250 ml). Trials comparing
Written informed consent by a competent operator intravenous saline versus bicarbonate prehydration
following discussion of potential complications is have failed to demonstrate any advantage of one
mandatory prior to the procedure (see Complications agent over the other. We recommend the use of 0.9%
section). saline for periprocedural hydration in patients at risk
13:40:34
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24
of CIN. Patients are encouraged to drink clear fluids The right and left coronary arteries arise from the
freely in the periprocedural period. A risk score based corresponding coronary sinuses immediately above
on eight clinical variables proposed by Mehran et al. the aortic valve. The right coronary artery runs in
more than a decade ago has been validated in a recent the right atrioventricular (AV) groove until the crux
study as a reliable tool in predicting the risk of CIN in (the anatomical intersection of the right and left AV
ACS patients undergoing coronary angiography. grooves and the posterior interventricular groove).
Along its course the RCA supplies the sinoatrial and
atrioventricular nodes, the right atrium and right ven-
Anticoagulation tricle and frequently the inferoposterior wall of the
A careful review of the indication for anticoagula- left ventricle as it enters the posterior interventricular
tion and the risk of thrombosis from interruption of groove as the posterior descending artery (PDA) in
anticoagulant therapy should be made in all cases. over 80% of cases. This is referred to as a right dom-
In an elective setting the anticoagulant is tempor- inant circulation.
arily suspended where possible, although coronary The left main coronary artery (LMCA) runs a
angiography may be performed via the radial route short course (usually 5–10 mm) before bifurcating
in anticoagulated patients if necessary. Such cases into the left anterior descending artery (LAD) that
should be discussed with the operator and planned runs in the anterior interventricular groove and
on an individual patient basis. A meta-analysis of the left circumflex artery (LCx) which mirrors
studies that compared uninterrupted anticoagula- the course of the right coronary artery in the left
tion with interruption ± heparin bridging suggests AV groove. The LAD supplies most of the inter-
that coronary angiography may be safely performed ventricular septum through its septal perforating
by continuing warfarin therapy with a target INR of branches and the anterolateral wall of the left ven-
2.0–2.5. tricle from two or more diagonal branches. Obtuse
marginal branches arise from the LCx and supply
Antiplatelet Agents the posterolateral LV myocardium. In 10% of cases
There is no reason to discontinue antiplatelet therapy the LCx continues as the PDA (left dominant cir-
prior to diagnostic angiography. In instances where culation) in the posterior interventricular groove,
angiography may proceed to PCI it is mandatory to while in the remaining 10% of cases both the RCA
treat the patient with loading doses of antiplatelets and the LCx provide branches to the posterior
according to local protocols. interventricular groove (codominant circulation).
Many of these preprocedural checks are confirmed Typical coronary angiographic images are repre-
with a World Health Organisation (WHO) surgical sented in Figure 4.1.
check list.
Haemostasis and Postprocedural
Coronary Angiography Care of Access Site
Manual compression may be employed to gain
Image Acquisition, Analysis and haemostasis at the site of arterial puncture. The radial
Interpretation artery is more superficial and readily compressed by
Invasive coronary angiography is an accurate imaging a band applied around the wrist. Femoral punctures
modality to delineate luminal anatomy although, can be compressed by a FemoStop device if manual
unlike non-invasive CTCA, it cannot comment on the compression is not sufficient to achieve haemostasis.
arterial wall. Multiple views (projections) are acquired Intravascular or extravascular closure devices (such
by radiography by injecting iodinated contrast into as the AngioSeal™ or Proglide™ devices) are also
the coronary arteries whilst being mindful of mini- used routinely following femoral puncture and can
mising contrast and radiation exposure to the patient, help to achieve haemostasis earlier when compared
as a stenosis in the ‘lumenogram’ may be eccentric or to manual compression. The AngioSeal™ device
foreshortened and could otherwise be missed. This is was noted to be more expensive and resulted in a
especially true in bifurcation lesions. slight delay in the patient leaving the catheter suite,
13:40:34
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25
(a) (b)
(c) (d)
pre post
Figure 4.1 Diagnostic angiograms of (a) normal left coronary artery, (b) normal right coronary artery, (c) prepercutaneous and
postpercutaneous coronary intervention to left anterior descending artery and (d) a saphenous vein graft.
but facilitated early patient ambulation and caused of ‘patent’ haemostasis using specially designed com-
less patient discomfort compared to the FemoStop pression bands.
device.
Patency of the radial artery following angiography Compl ications
has been shown to be increased by the use of 5F versus These may occur during or after the procedure.
6F sheaths, administration of 5000 units of heparin Serious complications are rare with a reported cumu-
via the side port of the arterial sheath and a technique lative incidence of <0.5%.
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26
Major Adverse Cardiac Events (MACE) from skin rash to sudden unexplained haemodynamic
collapse during or after the procedure.
Death is rare after coronary angiography and has been
consistently noted to be around 0.1% in large regis-
tries, whilst the rate of myocardial infarction ranges Learning Points
from 0.06% to 0.17% depending on the location of • Invasive angiography is the gold standard test for
atherosclerotic disease. Emergency coronary artery delineation of coronary lumen anatomy.
bypass surgery is rarely indicated (<0.1%). Ischaemic • Written informed consent by a competent
stroke rates of 0.05–0.1% have been reported and can operator following discussion of potential
arise from catheter manipulation in an atheroscler- complications is mandatory prior to the
otic ascending aorta, catheter related thrombosis and procedure.
embolism, air embolism or vessel dissection.
• Coronary angiography is an extremely safe
procedure in experienced hands with an overall
Access Site Complications complication rate of 0.1–0.5%.
These occur more frequently following femoral • The use of radial arterial access for coronary
arterial access and include local haematoma (with or angiography has steadily increased and may
without retroperitoneal extension in 0.15%), pseudo confer a net clinical benefit by reducing the risk of
aneurysm, iatrogenic arteriovenous (AV) fistula and vascular complications.
rarely arterial thrombosis or embolisation. Sudden • Contrast induced nephropathy can be avoided by
haemodynamic collapse may be the first indicator of a appropriate prehydration and use of isoosmolar
retroperitoneal haematoma but this is often preceded contrast agents in high risk patients.
by persistent tachycardia with or without hypoten-
sion and flank pain. A tender, pulsatile mass with a
systolic bruit is commonly noted in pseudoaneurysm Further Reading
while a continuous bruit may be audible in cases of Abellas-Sequeiros RA, Raposeiras-Roubin S, Abu-Assi E,
AV fistula. Clinical suspicion should prompt urgent et al. Mehran contrast nephropathy risk score: Is it
Doppler ultrasound and/or CT imaging to establish still useful 10 years later? Journal of Cardiology. 2015;
67: 262–267.
the diagnosis. Urgent referral to a vascular surgical
unit is often indicated in such cases. Barbeau GR, Arsenault F, Dugas L, Simard S, Lariviere
MM. Evaluation of the ulnopalmar arterial arches with
Benign vasovagal episodes precipitated by femoral
pulse oximetry and plethysmography: comparison
sheath removal are reported in 5–6% of patients, espe- with the Allen’s test in 1010 patients. American Heart
cially if the patient is dehydrated, but rapidly respond Journal. 2004; 147: 489–493.
to intravenous fluid and atropine. Delaney A, Carter A, Fisher M. The prevention of
Local complications are less common follow- anaphylactoid reactions to iodinated radiological
ing radial access but include pseudoaneurysm and contrast media: a systematic review. BMC Medical
sterile granuloma caused by deposition and hyper- Imaging. 2006; 6: 2.
sensitivity reaction to the hydrophilic coating on the Fleisher LA, Fleischmann KE, Auerbach AD, et al. ACC/
surface of radial sheaths. The more serious complica- AHA guideline on perioperative cardiovascular
tion of compartment syndrome caused by local tis- evaluation and management of patients undergoing
sue compression from a radial haematoma occurs in noncardiac surgery. Circulation. 2014; 130: 2215–2245.
<0.01% of cases but can be limb threatening if not rap- Krone RJ, Johnson L, Noto T. Five year trends in cardiac
idly decompressed. It is heralded by the six Ps in the catheterization: a report from the Registry of the
affected limb: pulseless, painful, pale, paraesthesia, Society for Cardiac Angiography and Interventions.
paralysis and perishing cold. Catheterization and Cardiovascular Diagnosis. 1996;
39: 31–35.
NICE. Management of Stable Angina. NICE Guidelines CG
Contrast Complications 126. July 2011.
Complications related to the contrast agent include Patel MR, Bailey SR, Bonow RO, et al. ACCF/SCAI/AATS/
CIN and allergic reaction to the iodinated compounds AHA/ASE/ASNC/HFSA/HRS/SCCM/SCCT/SCMR/
(discussed above). Allergic manifestations may range STS 2012 Appropriate use criteria for diagnostic
13:40:34
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27
catheterization. Journal of the American College of myth exposed. Journal of Emergency Medicine. 2010;
Cardiology. 2012; 59: 1995–2027. 39: 701–707.
Ryan TJ. The coronary angiogram and its seminal Valgimigli M, Gagnor A, Calabro P, et al. Radial versus
contributions to cardiovascular medicine over five femoral access in patients with acute coronary
decades. Circulation. 2002; 106: 752–756. syndromes undergoing invasive management: a
Schabelman E, Witting M. The relationship of randomised multicentre trial. Lancet. 2015;
radiocontrast, iodine, and seafood allergies: a medical 385: 2465–2476.
MCQs
1. Coronary angiography is indicated in the following 4. Which of the following is FALSE?
scenarios EXCEPT: (a) The circumflex artery may supply the proximal
(a) Prior to aortic valve surgery in a 48 year old male interventricular septum
with bicuspid aortic valve (b) The PDA usually arises from the RCA
(b) In a 56 year old male with exertional angina (c) Diagonal branches usually supply the posterolateral
(c) New onset heart failure with severe global LV LV myocardium
impairment on echocardiography (d) The SA nodal artery arises from the proximal RCA
(d) Prior to balloon mitral valvuloplasty in a 29 year (e) The AV nodal artery is usually the last branch
old female with mitral stenosis of the RCA before it enters the posterior
(e) Following out of hospital cardiac arrest and good interventricular groove
neurological recovery 5. A 55 year old man is recovering on ITU following a
2. Which of the following is most useful in reducing the witnessed cardiac arrest. New onset atrial fibrillation
risk of contrast induced nephropathy? is noted on the ECG and a bedside echocardiogram
(a) 0.45% saline by intravenous infusion suggests moderate– severe LV systolic impairment
with pronounced anteroseptal hypokinaesia. Further
(b) 0.9% saline prehydration is most useful at evaluation is planned with invasive coronary angiog-
preventing CN raphy. Which of the following is the most appropriate
(c) 10% sodium bicarbonate by intravenous infusion step before the procedure?
(d) Intravenous furosemide infusion at a rate of 20 mg/ (a) Administer regular dose of diuretics
hour (b) Load with aspirin and clopidogrel orally
(e) Use of hyperosmolar contrast agents (c) Start loading dose of warfarin
3. The advantages of radial access for coronary angiog- (d) Administer intravenous prehydration with 1 l 0.9%
raphy include all except: saline over 2 hours
(a) Lower rate of access site bleeding (e) (b) and (d)
(b) Lower rate of bleeding requiring transfusion
(c) Early ambulation post procedure
(d) Shorter fluoroscopic screening time during
angiography
(e) Lower rate of pain and discomfort post procedure
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Section 1 Diagnosis
Bronchoscopy in the Cardiothoracic

Chapter
Sumit Chatterji and Pasupathy Sivasothy
Introduction In this chapter, the role of bronchoscopy in the

CICU, contraindications, preparation, procedural
In 1897 Gustav Killian, a German laryngologist, per-
considerations and potential complications will be
formed the first airway examination in a human, with
discussed.
a rigid oesophagoscope, to remove a piece of bone
lodged in a mainstem bronchus. The next milestone
occurred with Shigeto Ikeda in 1964 and the devel- Indications for Bronchoscopy
opment of the first flexible bronchoscope capable One can generally group the indications for bron-
of examining the airways down to subsegmental choscopy into diagnostic and therapeutic reasons,
bronchi. Flexible bronchoscopy (FB) has been used though there is often overlap. Examples of this include
clinically since 1966 and has largely replaced rigid haemoptysis, foreign body removal, central airway
bronchoscopy as the technique of choice for airway obstruction, tracheo-oesophageal fistula and removal
examination and intervention. It can be of significant of proximal sputum plugs. Studies suggest 65% to 79%
help in the diagnosis and management of pulmonary of bronchoscopies performed in the ICU setting are
pathology in severely ill patients in the cardiothoracic conducted on patients being mechanically ventilated,
intensive care unit (CICU). Intensivists, interven- and of these 47% to 75% have a therapeutic indication.
tional pulmonologists and cardiothoracic surgeons In one review of bronchoscopies performed in critic-
are typical operators in this setting. Given its wide- ally ill patients on an ICU, 45% were performed to
spread use, it may be surprising that its role, efficacy remove bronchial secretions, 35% for collecting sam-
and safety in critically ill patients has largely been lim- ples from the lower respiratory tract, 7% for airway
ited in the published literature to small case series and assessment, 2% for haemoptysis, 0.5% for assisting
expert opinions. A few meta-analyses have attempted difficult tracheal intubation and 0.5% for removing
to evaluate its role, particularly in the context of venti- foreign bodies.
lator acquired pneumonia. Indications for bronchoscopy in a CICU are sum-
Patients in a CICU are typically selected for pre- marised in Table 5.1.
dominantly cardiac or respiratory support, with over
40% on mechanical ventilation. Patients are varied and Orotracheal Intubation
include recipients of heart/lung transplants, immuno-
compromised established transplant recipients, those Difficult Intubation
receiving anticoagulation or multiple antiplatelet FB can be useful to facilitate difficult endotracheal
agents, and those with chronic cardiac or respiratory intubations in patients with a Cormack–Lehane score
disease. Polypharmacy is common, with the poten- of 3 or more, limited mobility of head and neck, cer-
tial for multiple drug interactions adding to issues vical spine fractures, or where severe coagulopathy
facing the bronchoscopist, which need to be carefully or excessive secretions might make intubation with
evaluated before deciding to proceed. Determining a layngoscope inadvisable. Despite its advantages in
the appropriateness of the procedure, then optimis- these situations, it is typically only used in a small
ing the patient and environment to ensure a safe and proportion (0.07–3.4%) of patients in the ICU set-
effective intervention, depends on a multidisciplinary ting. The oral route is preferred as a larger diameter
approach with the physician/ surgeon, intensivists, endotracheal tube (ETT) can be passed. Adult bron-
interventional pulmonologist and nurses all involved. choscopes have a diameter of approximately 6 mm,
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Chapter 5: Bronchoscopy
Table 5.1 Indications for bronchoscopy in a CICU ETT cuff is deflated and the bronchoscope/new ETT
Primarily diagnostic passed through the vocal cords alongside the old ETT.
• Pneumonia (nosocomial, ventilator associated, The old ETT is then withdrawn and the new tube
immunocompromised host) adjusted accurately under direct vision prior to cuff
• Acute inhalational injury or burns inflation.
• Assessment for airway trauma (post blunt or penetrating
thoracic injury) Controlled Extubation
• Localised wheeze or stridor
• Diffuse or focal lung disease (infiltrates or mass lesions)
Patients with suspected upper airway obstruction are
• Assessment of bronchial stump or anastomosis ideal candidates for FB directed extubation. Examples
• Assessment of graft rejection (transbronchial lung biopsies) include bilateral vocal cord paralysis, tracheomalacia
Primarily therapeutic or tracheal stenosis due to causes such as multiple
• Airway management (difficult intubation, double lumen intubation attempts, prolonged intubation or airway
endotracheal tube placement, endotracheal tube injury. The bronchoscope is inserted into the ETT
replacement) just beyond the tip, the cuff deflated and the bron-
• Atelectasis (lobar or whole lung) due to proximal choscope/ETT slowly removed en bloc. During with-
mucus plug
drawal, if there is endoscopic evidence of significant
• Airway foreign bodies
subglottic or glottic obstruction, the ETT can be safely
• Massive haemoptysis
• Strictures and stenoses (balloon dilatation and stents)
reinserted under direct vision.
• Central airway obstruction due to tumour (cryodebulking,
electrosurgery, laser)
• Tracheo-oesophageal fistula (stenting)
Diagnosis of Respiratory Infection in
• Bronchopleural fistula (fibrin glue, endobronchial valve Ventilated Patients
insertion)
• Percutaneous dilational tracheostomy insertion Ventilator Associated Pneumonia (VAP)
Pneumonia is the most common infection in the
CICU. The overall incidence of VAP ranges from 9%
able to pass through a size 7.5 ETT or larger –typical to 25% in the general ICU population, with rates up to
sizes used in adult patients. To prevent damage to the 70% in those with acute respiratory distress syndrome
bronchoscope, a bite block is advised. As four minutes (ARDS). The risk increases over the first 10 days and
or more must be allowed to accomplish intubation, can affect two thirds of patients who have been ven-
this technique is not recommended for apnoeic or tilated for more than 30 days. Mortality ranges from
near apnoeic patients. 35% to 90%. Bronchoscopically directed lavage, pro-
tected brushing and occasionally deep lung biopsies
Double Lumen Endotracheal Tubes (transbronchial lung biopsies) are often used to deter-
FB can be used to assist placement of a double lumen mine the cause of infection. Qualitative or quantita-
ETT used for differential ventilation or management tive (number of colony forming units, or number of
of massive haemoptysis. A thin 4 mm diameter bron- intracellular organisms) techniques can be used to
choscope can pass through a 35F double lumen tube; analyse the samples obtained. This results in a wide
the smallest size used in adults. range of reported sensitivities of bronchoscopic tech-
niques (51–100%) with the overall impression that
Changing Endotracheal Tubes bronchial lavage and brushing are safe techniques
Occasionally an ETT may need to be changed due for microbiological diagnosis in ventilated patients.
to cuff leakage or to facilitate a bronchoscopic inter- However, well- conducted systematic reviews look-
vention. If endotracheal reintubation is expected to ing at bronchoscopic versus ‘non-invasive’ techniques
be difficult, a flexible bronchoscope may be used to (tracheal suctioning, blind catheter brushing) in redu-
facilitate the exchange as an alternative to a bougie. cing mortality and ICU stay in clinically diagnosed
The stomach contents are aspirated via a nasogastric VAP patients have shown no statistically significant
tube, following which the new ETT is inserted over differences in mortality, duration on mechanical
the bronchoscope and inserted into the posterior ventilation, length of ICU stay or antibiotic change.
pharynx, whilst suctioning secretions. The existing The British Thoracic Society therefore recommends
13:41:59 29
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30
directed non-invasive diagnostic strategies in prefer- • Failure to respond to chest physiotherapy and
ence to bronchoscopy in ventilated patients suspected other measures;
to have VAP. • Where physiotherapy or repositioning is not
feasible (e.g. thoracic trauma, spinal fractures)
Immunocompromised Patients • Patients with neuromuscular disorders and
Patients with solid organ transplants receiving impaired cough;
immunosuppressive medications in the CICU are at • Cystic fibrosis patients (copious inspissated
higher risk of developing opportunistic fungal infec- secretions);
tions, including Pneumocystis jirovecii, invasive asper- • Lung transplant patients with tenacious plug
gillosis, candidiasis, cryptococcus, bacterial infections composed of necrotic tissue and mucus.
and viral infections such as cytomegalovirus. In areas
of high prevalence in the UK, or in patients from
endemic areas worldwide (Sub-Saharan Africa, Far Diagnosis and Management of
East, Southeast Asia, parts of Eastern Europe and Haemoptysis
South America), tuberculosis must also be excluded. Bronchoscopy in conjunction with CT can be useful to
Bronchoalveolar lavage (BAL) with 120–200 ml of identify the endobronchial source of haemoptysis in
instilled 0.9% saline can be performed via the bron- intubated patients with persistent or excessive bleed-
choscope into an affected lobe. If diffuse changes are ing from the ETT. It is also typically employed (usually
present, bilateral BAL (preferentially of the upper through an ETT) for diagnosis and control of massive
lobes) appears to provide the highest sensitivity. BAL haemoptysis, defined as 400 ml in 24 hours, or 200
is reported to have sensitivity for P. jirovecii of 90–98% ml in any one event. Through the bronchoscope, iced
and is considered the gold standard. Diagnostic sen- saline, fibrin precursors or topical adrenaline 1/10,000
sitivity for pulmonary tuberculosis can be increased can be instilled to attempt haemostasis in a bleeding
from up to 30% based on microscopy alone to 86% segment. Alternatively, the bronchoscope can be used
with rapid PCR techniques, and is preferable to to facilitate the passage of specific endobronchial
transbronchial lung biopsies in the majority of ICU blockers (e.g. Cohen flexitip® or Arndt®) and a Fogarty
patients due to the potential risk of pneumothorax or or Swan-Ganz catheter to occlude the bleeding lobe
bleeding. For patients with suspected invasive asper- or segment. Finally, an ETT can be directed broncho-
gillosis, BAL galactomannan testing has shown super- scopically into the normal lung to isolate the bleeding
iority to fungal staining and culture, with sensitivity of side and avoid spillover of blood, or help direct a dual
94% and specificity of 79% and should be considered lumen ETT to achieve the same effect. Where facilities
if available. and expertise exist, rigid bronchoscopy may be pref-
erable in cases of massive haemoptysis as it provides
Managing Lobar or Whole Lung Atelectasis a secure airway, large volume suction capability and
FB has been used in ventilated patients with lobar or easy access to the airways with endobronchial block-
whole lung atelectasis who have failed to respond to ing devices. All these measures attempt to secure the
treatments such as physiotherapy, nebulised saline, airway, ensure adequate oxygenation, prevent soiling
mucolytics or repositioning (including prone venti- of the normal lung and in some cases allow definitive
lation). In several small case series it has been shown airway intervention –or buy time for a surgical or
to be effective in immediate reversal of lobar atelec- interventional radiology solution.
tasis. Physiotherapy and conventional non-invasive
measures are still recommended first line treat- Thoracic Trauma
ment with bronchoscopy reserved for the following Tracheobronchial injuries affect up to 2.8% of severe
situations: blunt chest trauma and accidental deaths. Sternal or
• Life threatening whole or near-whole lung upper rib fractures can indicate significant blunt force
collapse; injury and likelihood of internal problems so bron-
• Lobar atelectasis due to proximal sputum plug choscopic examination is mandatory. Physical and
with a lack of visible air bronchograms on radiological signs include hypoxaemia, haemoptysis,
radiology; pneumothorax, surgical emphysema, haemothorax,
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31
pneumomediastinum, flail chest and the so- called atelectasis, ARDS, central airway obstruction, obesity,
‘falling lung sign’ on chest radiograph (pneumothorax hypotension), the effects of sedation and the pro-
with atelectatic lung collapsing away from the medias- cedure being undertaken (such as suctioning to clear
tinum) which is pathognomonic of rupture of a main- airway debris).
stem bronchus. All these factors need consideration prior to under-
taking FB, and in intubated patients particular atten-
Persistent Bronchopleural Fistula (BPF) tion needs to be paid to ensuring an adequate sized
airway and choosing an appropriately sized broncho-
The incidence of BPF after pulmonary resection var- scope for the task (a thinner scope may be safer but
ies between 4.5–20% after pneumonectomy and 0.5% will have less suctioning capacity and may not allow
after lobectomy. Risk factors for this serious complica- passage of certain instruments such as a cryoprobe).
tion include right-sided pneumonectomy, a long bron- Table 5.2 summarises the main physiological
chial stump, residual cancer at the bronchial margin, effects of bronchoscopy in intubated patients.
devascularisation of the bronchial stump, prolonged
ventilation and reintubation after resection. Many
patients may not be fit enough to have repeat sur-
Procedures Performed with
gery where intercostal drainage and sometimes pleu- Bronchoscopy
rodesis methods fail. The extent of the air leak may Flexible bronchoscopes typically have working chan-
prevent lung reinflation and delay ambulation, even nels 2.0–3.2 mm in diameter, allowing varying suction
with Heimlich valves or portable suction devices (e.g. capacity or ability to pass specialised instruments to
Thopaz®, Medela Switzerland). Bronchoscopy can be perform interventions.
used in these patients to identify the predominant Additionally, linear endobronchial ultrasound
lobe/segment causing the air leak (by employing an scopes available today (with approximate external
endobronchial occluding balloon), followed by inser- diameter 6.9 mm) can be used via larger ETTs to
tion of one-way valves preventing airflow into that seg- facilitate transbronchial needle aspiration of medias-
ment. Examples of valves used for this purpose include tinal lymph nodes or masses.
Emphasys® (Pulmonx, Redwood, USA), Spiration Advanced bronchoscopic interventions are gener-
IBV® (Olympus Medical, Japan) or Watanabe spigots® ally the remit of the interventional pulmonologist or
(Novotech, France). These devices require consid- thoracic surgeon.
erable expertise to deploy accurately and are usually Procedures likely to be encountered in the CICU
inserted by interventional pulmonologists. are detailed in Table 5.3.
Physiological Effects of Bronchoscopy Contraindications to Bronchoscopy

In the non-intubated adult patient, a standard 5.7 mm There are very few absolute contraindications to per-
diameter bronchoscope occupies only 10% of the forming FB. Among these are non-cooperation or
cross-sectional area of the trachea. Therefore, in spon- refusal by the awake patient, operator inexperience,
taneously breathing patients endotracheal pressures lack of suitable equipment and the inability to main-
generated are similar to those in patients without tain adequate oxygenation during the procedure.
bronchoscopy. The remainder are considered relative contrain-
In an intubated, ventilated patient, the effect is dications as they place the patient at risk of certain
quite different. The obstructive effect of the broncho- complications. FB in these settings should be weighed
scope is added to that of the ETT, with the potential to carefully against potential risks to the patient.
cause quite dramatic changes in respiratory mechan- Hypoxaemia defined as an inability to maintain SpO2
ics, gas exchange and haemodynamics. Indeed, a > 90% can predispose to arrhythmias through myocar-
5.7 mm bronchoscope occupies 40% of the cross- dial ischaemia and recent acute coronary syndromes
sectional area of a 9.0 mm inner diameter ETT, 51% of increase the risk of fatal myocardial ischaemia.
a 8.0 mm ETT and 66% of a 7.0 mm ETT. Relative contraindications include:
Complicating the effect of the bronchoscope on • Severe hypoxaemia with CPAP or FiO2 >0.5 to
the patient’s physiology are patient-specific factors achieve a PaO2 >9.0 kPa;
including the underlying diagnosis (for example, • Acute coronary syndrome within 4 weeks;
13:41:59 31
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32
Table 5.2 Effect of bronchoscopy on respiratory physiology in the ventilated patient
Outcome Additional notes

Respiratory mechanics Increased VT reduction 200–300 ml with suctioning
• PEEP (10–15 cmH20, up to 35 cmH20) Main determinants of effect are ETT internal diameter,
• Peak inflation pressures (up to 80–90 cmH20) bronchoscope external diameter and duration of
• FRC (30%) suctioning
Cough can further exacerbate peak airway pressures
Reduced
risking barotrauma
• VT
Auto-PEEP can develop leading to raised FRC, reduced
• FEV1 (40%, bronchospasm can exacerbate)
FEV1 and expiratory tidal volumes
• PEEP (with suction)
• FRC (with suction)
Gas exchange Increased Suction can reduce PaO2 by 40%. Mechanisms include
• PaCO2 (average 1 kPa) atelectasis, small airway collapse, reduced VT, reduced FRC
• PaO2 (in some cases with secretion clearance and increased V/Q mismatch
or due to auto-PEEP recruitment) Low FEV1, prior LTOT, raised BMI and significant
comorbidities are risk factors for an exaggerated response
Reduced
• PaO2 (average 2.5 kPa)
• SpO2 (>5% desaturation in over 65% cases)
• SpO2 falls below 90% in at least 20% cases
Haemodynamics Increased Sympathetic stimulation due to hypoxaemia, hypercapnia
• Heart rate and mechanical irritation of the airways
• Mean arterial pressure Raised ICP potentially caused by a combination of
• Cardiac output hypoxaemia, hypercapnia and cough with auto-PEEP. Is
• Pulmonary artery pressure usually compensated by the raised mean arterial pressure
during the procedure
• Intracranial pressure (can increase >100%)
Reduced
• Mean arterial pressure (if significant
auto-PEEP)
• Uncontrolled arrhythmia; coagulation parameters must be within safe limits. If

• Systolic blood pressure <90 mmHg despite on warfarin for a metallic heart valve, discuss with the
vasopressors; cardiologist and typically discontinue and cover with
• Uncontrolled bronchospasm; low molecular weight heparin (LMWH) until the INR
• Auto-PEEP >15 cmH20; is below 1.5 (omitting the LMWH dose 24 hours prior
• Bleeding diathesis (thrombocytopenia <20– to bronchoscopy). For other indications, warfarin
50 × 109/l, INR >1.5, clopidogrel, newer oral may be stopped or partially reversed with vitamin
anticoagulants (NOAC), chronic renal failure); K if a biopsy is planned. Clopidogrel should also be
• Severe pulmonary arterial hypertension; discontinued 7 days prior where possible as there is a
• Intracranial hypertension. significant risk of bleeding with biopsies. NOACs can
be stopped 48 hours prior. Review the list of relative
and absolute contraindications to consider whether
The Bronchoscopy Procedure the procedure can be safely deferred.
Preparation The Equipment

A working sterilised video bronchoscope of appro-
The Patient priate diameter and monitor/stack is required. It can
Ensure the patient is correctly identified and consent be difficult to position the equipment around a bed
obtained if feasible. Radiology must be reviewed to space when there are other pieces of equipment in
identify the reason for the procedure and a target area the vicinity. The best position involves the operator
for sampling or intervention. The full blood count and on one side of the bed, facing the monitor/stack on
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Table 5.3 Bronchoscopic procedures performed in the CICU
Procedure Basic or advanced Indications Requirements

Bronchial wash Basic Bronchial clearance and sampling Platelet count >20
Bronchoalveolar lavage Basic Cytological and microbiological Platelet count >20
sampling
Bronchial brush Basic Cytological and microbiological Platelet count >50
sampling INR <1.5
Bronchial biopsy Basic Histological and microbiological Platelet count >50
sampling INR <1.5
Foreign body extraction Basic/Advanced Removal of airway foreign body Platelet count >50
INR <1.5
Working channel diameter >2.6 mm
(for larger forceps or retrieval baskets)
Transbronchial biopsy Advanced Histological and microbiological Platelet count >50
sampling INR <1.5
Cryotherapy Advanced Freezing/extraction of Platelet count >50
endobronchial tissue or debris INR <1.5
Diathermy Advanced Tissue debridement Platelet count >50
Haemostasis INR <1.5
Insulated scope
Avoid FiO2 >0.4 (risk of airway fire)
Care with pacemakers
Earth electrode pad
Balloon dilatation Advanced Intrinsic or mixed benign or Platelet count >50
malignant airway narrowing INR <1.5
Stenting Advanced Malignant or benign airway stenosis Platelet count >50
INR <1.5
Some operators prefer fluoroscopy
Endobronchial ultrasound Advanced Sampling mediastinal or hilar nodes/ Platelet count >50
mass INR <1.5
Size 9.0 ETT if intubated
Endobronchial valves Advanced Persistent bronchopleural fistula Platelet count >50
INR <1.5
the other side. If fluoroscopy is needed, the patient signs and electrocardiogram should be continuously
will need to be transferred onto a screening trolley, monitored during and after the procedure. Consider
which allows access to a ‘C arm’ imaging device. All end-tidal CO2 monitoring in hypercapnic patients.
bronchoscopic accessories required for the procedure
should be assembled. For patients with an ETT (or Personnel and Skills
tracheostomy) being ventilated, a ‘swivel adaptor’ is Typically, in the CICU, a bronchoscopy requires the
connected between the tube and ventilator tubing bronchoscopist, an anaesthetist (to separately monitor
to allow bronchoscope access without losing venti- sedation and ventilation parameters), a nurse assisting
lation pressure (see Figure 5.1). For those not being the bronchoscopist and a further nurse to control the
invasively ventilated, ensure an appropriate mode of position of the ETT/tracheostomy or provide general
delivery of ventilation or oxygen is established (e.g. a support for the procedure. The bronchoscopist and
Venturi mask, CPAP or non-invasive ventilation full their nursing assistant should have the requisite com-
face mask, laryngeal mask airway). The patient’s vital petency to perform the intended procedures and be
13:41:59 33
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34
(a) (b)
Figure 5.1 Bronchoscopy swivel catheter mount. (a) Close up image of the bronchoscope entering the catheter mount via a self-sealing soft
rubber ring. This allows for reduced air leakage during bronchoscopy of an invasively ventilated patient. (b) Bronchoscope entering the catheter
mount and passing via the endotracheal tube (ET). To ensure smooth passage down the ET tube, lubricant is applied to the outside of the
bronchoscope. (A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)
familiar with the equipment and devices used. They demonstrated this can be an effective option
must also be able to deal efficiently with potential in patients in respiratory failure with PaO2/
complications. FiO2 <300 and can be well tolerated by patients.
A full face mask or hood can be used with the
Precautions bronchoscope accessing the mask through a
All staff should wear personal protective equipment. swivel adaptor attached to the front of the mask
At the very least gloves, an apron, face mask and eye (see Figure 5.2).
shield. For patients with potentially transmissable dis-
eases through aerosolisation, an FFP3 or respirator With General Anaesthesia
face mask should be used and local infectious disease
• Laryngeal mask airway. This can be useful for
control guidance sought where needed.
complex procedures (e.g. airway debridement,
The bronchoscope should be lubricated with
stenting) where the bronchoscope is withdrawn
sterile gel to facilitate easy passage and reduce the risk
and reinserted repeatedly.
of damage.
• ETT. Most patients in the CICU will be
Ventilation and Oxygenation Options mechanically ventilated by ETT. The internal
Adequate ventilation during bronchoscopy aims to diameter of the ETT should be at least 2 mm
achieve a consistent SpO2 >90% with patient comfort larger than the external diameter of the
and normal haemodynamics. If the procedure is likely bronchoscope to permit effective ventilation
to be complex and prolonged, or have significant risk and prevent scope damage. The ETT should
of airway compromise, invasive ventilation or a laryn- also be withdrawn as necessary to allow the
geal mask airway should be considered –or in some bronchoscope easy access to both main bronchi.
cases rigid broncoscopy in theatre. If invasively venti- • Tracheostomy. The internal diameter of the tube
lated, the patient is preoxygenated with FiO2 1.0 start- (usually quoted as the internal diameter of the
ing 10 minutes preprocedure. outer tube if an inner tube is also present) must
be 2 mm greater than the external diameter of
the scope. A standard adult bronchoscope with
With Conscious Sedation external diameter 5.5–6.2 mm should safely fit
• Self-ventilating with oxygen delivered by nasal in a size 8–10 tracheostomy tube. The inner tube
cannulae or a face mask (Venturi or Hudson). should be removed if present and the 15 mm
• Self-ventilating on CPAP or non-invasive connector attached to a swivel adaptor. Special
ventilation (NIV) with oxygen. Studies have care should be taken during scope withdrawal
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(a) (b)
Figure 5.2 Bronchoscopy during non-invasive ventilation using modified full face masks (a) via the oral approach using a bite block and
(b) via the nasal approach. (A black and white version of this figure will appear in some formats. For the colour version, please refer to the
plate section.)
to prevent tube displacement or shearing of the patients, lung transplant recipients, renal or hepatic
scope on the distal end of the tracheostomy tube. disease, malnutrition, platelet dysfunction or those
Fenestrated tubes can pose particular risks in this with acquired coagulopathies.
regard. Other risks include pneumothorax (7–15% with
lung biopsies), significant cardiac arrhythmia (3–
The Procedure 5%), oxygen desaturation, which may persist for sev-
eral hours postprocedure (especially in patients with
In spontaneously breathing patients on oxygen, or
ARDS), bronchospasm and haemodynamic instability.
CPAP/ NIV, the upper airway is anaesthetised with
Postbronchoscopy fever occurs in 5–16% of patients
lidocaine spray and the nostrils with lidocaine gel.
due to release of inflammatory mediators a few hours
Care must be taken with lidocaine dosing in the eld-
after the procedure and is self-limiting. Finally, one
erly and those with cardiac, hepatic or renal impair-
must also be aware of the effect of medications used
ment. Although up to 15.4 mg/ kg has been used
during the procedure. Lidocaine toxicity may present
without adverse effects, mild forms of lidocaine toxicity
with tremulousness, shivering, dizziness and progress
have also been reported with doses above 9.6 mg/kg.
to sedation, unconsciousness, and convulsions fol-
The British Thoracic Society recommends a dose not
lowed by cardiorespiratory collapse. Blood concen-
exceeding 8.2 mg/kg ideal body weight. Effective cough
trations after topical application may be 30% of that
suppression can be associated with total lidocaine dose
obtained by rapid intravenous administration. In the
<160 mg and the aim should be to use the lowest dose
ventilated patient, early features may not be clinically
to achieve the desired effect. The dose used must always
apparent and therefore care must be exercised with
be documented. The transnasal approach is contrain-
dosing and the operator vigilant for signs of toxicity.
dicated in patients with coagulopathy due to the risk of
epistaxis. The oral approach requires a mouth guard to
prevent biting of the bronchoscope. A summary of the
process in ventilated patients is given in Table 5.4. Learning Points
• Flexible bronchoscopes typically have an external
Complications of Bronchoscopy diameter 5.5–6.2 mm with working channel 2.0–
Reported complications of FB in the ICU are less 3.2 mm. Be familiar with local equipment. Some
than 10% with a mortality rate 0.01–0.05%. Death instruments require a larger working channel.
from bleeding ranges from 0.03% to 0.05% and is • The inner diameter of an ETT must be at least
usually confined to those undergoing biopsy (typ- 2 mm larger than the external diameter of the
ically transbronchial lung biopsy) procedures. The bronchoscope. Replace the ETT or use a smaller
risk of bleeding is increased in immunocompromised bronchoscope if necessary.
13:41:59 35
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36
Table 5.4 Summary of the bronchoscopy process in ventilated patients
1 Ensure ETT/tracheostomy internal diameter >2 mm larger than diameter of bronchoscope. Change if needed, or consider using a
thin/paediatric scope if necessary.
2 Attach a swivel adaptor to the 15 mm connector.
3 Increase sedation and consider opiate antitussive or muscle relaxants.
4 FiO2 increased to 1.0 starting 10 minutes prior to procedure. Unless life-saving, postpone bronchoscopy if SpO2 remains <90%.
5 Mandatory ventilation mode used. Volume control may result in unacceptably high peak airway pressures. Pressure controlled
modes require an increase in peak pressure setting.
6 Aim for tidal volume (TV) 6–8 ml/kg ideal body weight.
7 PEEP stopped or reduced by 50% during the procedure.
8 Lubricate the scope well with sterile gel and insert through the swivel adaptor into the airway. An assistant should hold the ETT
throughout the procedure.
9 Instill 2 ml aliquots of 1–2% lidocaine to trachea, carina, right and left bronchial tree.
10 Use suction sparingly and no more than 3 seconds each time.
11 If using diathermy or laser in the airway, ensure the FiO2 is < 0.4 to minimise the risk of airway fire.
12 Monitor blood pressure, pulse, electrocardiography, oximetry, end-tidal CO2, sedation, VT and peak airway pressures throughout
the procedure.
13 If oxygenation cannot be maintained, or there is haemodynamic instability, the procedure must be terminated and the patient
stabilised.
14 Check the position of the ETT at the end of the procedure.
15 Wean FiO2 and reinstate preprocedure ventilation parameters after the procedure.
16 A chest X-ray after bronchoscopy is important to exclude complications including pneumothorax and to assess the result of an
intervention.
• Physiological effects are variable but generally British Thoracic Society Interventional Bronchoscopy
include increased PEEP, FRC and airway Guideline Group. British Thoracic Society
pressures, with reduction in SpO2, VT and FEV1. guideline for advanced diagnostic and therapeutic
flexible bronchoscopy in adults. Thorax. 2011; 66:
Parameters need continuous monitoring and
1–21.
ventilation settings adjusted where appropriate.
Chen A, Kollef MH. Bronchoscopy in the intensive care
• Unless for life-saving intent, bronchoscopy
unit. In: Wang K-P, Mehta AC, Turner JF (Eds).
must not be performed where SpO2 cannot be Flexible Bronchoscopy, 3rd Edition. Oxford: Wiley-
maintained >90% with FiO2 1.0. Blackwell, 2012. doi:10.1002/9781444346428.ch24
• Be alert to signs of local anaesthetic toxicity. Du Rand IA, Blaikley J, Booton R, et al. British Thoracic
Use the lowest effective dose and no more than Society guideline for diagnostic flexible bronchoscopy
8.2 mg/kg ideal body weight. Document the in adults. Thorax. 2013; 68: 1–44. doi:10.1136/
dose used. thoraxjnl-2013–203618
Estella A. Bronchoscopy in mechanically ventilated
Further Reading patients. In: Haranath SP (Ed). Global Perspectives on
Bronchoscopy. InTech, 2012. http: //cdn.intechopen.
Antonelli M, Conti G, Rocco M, et al. Noninvasive
com/pdfs/37333/In Tech-Bronchoscopy-in_
positive-pressure ventilation versus conventional
mechanically_ventilated_patients.pdf.
oxygen supplementation in hypoxemic patients
undergoing diagnostic fiberoptic bronchoscopy. Chest. Khalil A, Soussan M, Mangiapan G, et al. Utility of
2002; 121: 1149–1154. high-resolution chest CT scan in the emergency
management of haemoptysis in the intensive care
Bion JF, Barrett H; CoBaTrICE Collaboration, European unit: severity, localization and aetiology. British Journal
Society of Intensive Care Medicine. Development of Radiology. 2007; 80: 21–25.
of core competencies or an international training
programme in intensive care medicine. Intensive Care. Kreider ME, Lipson DA. Bronchoscopy for atelectasis in
2006; 32: 1371–1383. the ICU. Chest. 2003; 124: 344–350.
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Krell WS. Pulmonary diagnostic procedures in the Raoof S, Mehrishi S, Prakash UB. Role of bronchoscopy in
critically ill. Critical Care Clinics. 1988; 4: 393–407. modern medical intensive care unit. Clinics in Chest
Lindholm C, Ollmann B, Snyder J, Millen E, Grenvik Medicine. 2001; 22: 241–261.
A. Cardiorespiratory effects of flexible fiberoptic Toma TP, Kon OM, Oldfield W, et al. Reduction of
bronchoscopy in critically ill patients. Chest. 1978; persistent air leak with endoscopic valve implants.
74: 362–367. Thorax. 2007; 62: 830–833.
Olopade CS, Prakash UBS. Bronchoscopy in the
critical care unit. Mayo Clinic Proceedings. 1989;
64: 1255–1263.
MCQs
1. Which of the following is true during bronchoscopy in (d) Paediatric bronchoscope
a ventilated patient? (e) Rigid bronchoscope
(a) Tidal volume is reduced 4. When undertaking a bronchoscopy via a tracheos-
(b) PEEP is reduced during suctioning tomy which one of the following is correct?
(c) PaO2 can rise in some scenarios (a) The tracheostomy tube should have an internal
(d) Mean arterial pressure can be reduced diameter >2 mm compared to the bronchoscope
(e) All of the above (b) The inner tube should remain in situ
2. Which of the following is NOT a relative contraindica- (c) No additional considerations are needed if the tube
tion for bronchoscopy? is fenestrated
(a) Tachyarrhythmia (d) Additional sedation is routinely required in add-

ition to topical local anaesthetic
(b) PEEP >15 cmH2O
(e) A swivel adaptor is not required in this setting
(c) Aspirin
5. Which of the following cannot be done directly via the
(d) INR >1.5 or platelets <20 × 109/l working channel of the flexible bronchoscope?
(e) Intracranial hypertension (a) Bronchial biopsy
3. Which of the following will fit down a double lumen (b) Endobronchial valve placement for bronchopleural
endotracheal tube? fistula
(a) Linear EBUS (endobronchial ultrasound) scope (c) Cryotherapy
(b) Standard bronchoscope with outer diameter (d) Bronchial stent placement
of 5.7 mm
(e) Foreign body extraction
(c) Interventional bronchoscope with outer diameter
of 6.2 mm
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Section 1 Diagnosis
Microbiology Testing
Chapter
6 A Ruth M Kappeler and Margaret I Gillham
Introduction enable appropriate sampling of patients and as short a

time as possible to sample processing whether the unit
Infections in cardiothoracic intensive care units are
has an on-site or off-site laboratory. There should be
common, either as the primary presenting illness as in
24 hour access to the laboratory for handling urgent
the case of infective endocarditis or severe respiratory
samples and for viewing results. Furthermore, round-
failure, or as a secondary complication of cardiothor-
the-clock accessibility to infection specialists is crucial
acic procedures. Moreover, infectious complications
to ensuring correct test selection, timely reporting,
are known to impact on morbidity and mortality.
interpretation of microbiology results, infection con-
The sites of infection encountered include surgical
trol and antimicrobial advice.
site infections (including organ space), device related
infections (prosthetic valve endocarditis, ventricular
assist device infections), bloodstream infections, line Ordering of Tests
related infections, respiratory tract, gastrointestinal Most hospitals use an electronic ordering system for
tract and urinary tract infections. pathology requests, including those for microbiology.
The time taken to identify microorganisms in clin- Testing protocols can be set up to ensure that the appro-
ical samples can have an impact in the management priate range of tests is ordered for different clinical
of patients with sepsis. Best practice in collection and scenarios. For example, patients admitted with severe
timely processing of microbiological samples is essen- respiratory failure for ECMO will require extensive
tial, not only to ensure optimal antimicrobial manage- testing on admission to critical care (see Table 6.1 for
ment and thereby outcome, but also to ensure optimal guidance on test selection for this scenario) whereas
infection control management of patients within car- patients admitted for elective cardiac surgery, who
diothoracic units. The ability to culture organisms from have no complications, will only require preoperative
clinical samples is affected by type and quality of the spe- screening samples. Electronic ordering systems can be
cimen, prior antibiotic therapy, transportation, storage set up as specimen or sample type based. It is important
conditions of samples and time to sample processing. to ensure from the outset that the way the system is con-
Emerging technologies are enabling faster identification figured not only allows ease of ordering for the clinical
and quantification of pathogens, resulting in more rapid user but also includes a degree of demand management
diagnostics. This has the potential not only to affect to reduce inappropriate testing. Electronic test order-
patient outcome but also to ensure better antimicrobial ing also allows the development of testing sets whereby
stewardship by enabling targeted antimicrobial therapy a standard protocol for microbiology testing can be
and avoidance of unnecessary antimicrobial use which agreed according to the patient’s circumstances, and the
can lead to adverse effects for patients and encourage same testing strategy can be followed each time. This
development of resistance in bacteria. It is necessary can be beneficial in cases of severe respiratory failure
to perform a systematic physical examination before on ECMO where an infective cause is suspected or for
requesting diagnostic tests as this will enable test selec- patients who develop postoperative sepsis.
tion and avoid unnecessary sampling.
The importance of microbiological diagnostics to Correct Sampling Procedures
cardiothoracic units cannot be underestimated and General principles apply to collection of all micro-
units need to ensure that processes are in place to biology samples. They should be collected at the correct
13:43:27
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39
Chapter 6: Microbiology Testing
Table 6.1 Suggested testing set for patients with severe that the correct procedures are followed so that sam-
respiratory failure requiring ECMO ples are transported safely and in a timely manner to
Baseline tests the laboratory. Samples requiring immediate atten-
Sample Organism tion for processing should be notified to the labora-
tory in advance and identified as urgent. All samples
Blood Human immunodeficiency
(HIV) virus should be transported with completed information
Herpes simplex virus (HSV) IgG identifying the patient, time and date collected, tests
and PCR required and antibiotic history. This may be in bar
Cytomegalovirus (CMV) IgG and PCR code format or with a physical request form. Samples
N. meningitidis PCR with risk of infection should be identified by the clin-
Pneumococcal PCR ical user and visible to the laboratory handling the
Mycoplasma and chlamydia sample. Where possible, samples should be collected
serology
prior to antibiotic therapy but this should not lead
Blood cultures
to delays in managing the patient or administering
Bronchoalveolar lavage Respiratory virus PCR
antibiotics.
CMV, HSV, adenovirus PCR
Hand hygiene should be performed before and
Pneumocystis jirovecii PCR
Galactomannan
after specimen collection. Personal protective equip-
Legionella culture and PCR ment (gloves, waterproof apron) is required during
Mycoplasma pneumoniae PCR specimen collection when contact with bodily flu-
Chlamydophila pneumoniae PCR ids is anticipated. Masks may be required for collec-
Smear and culture for tion of respiratory samples, for example with sputum
Mycobacterium tuberculosis induction.
Fungal culture Blood cultures are taken when bacteraemia is sus-
Routine culture pected and should be taken via a dedicated venepunc-
Nose and throat viral Respiratory virus PCR ture, peripherally, rather than through an existing
swab Consider pernasal swab for pertussis line. Where endocarditis or device related infection
Urine sample Culture is suspected, up to three sets can be taken at separate
Legionella antigen times over a 24 hour period. However, it is the actual
Pneumococcal antigen
volume of blood that is important, therefore inocu-
lating one bottle with the correct volume of blood is of
Additional tests
greater value than sharing the blood volume between
Risk factor/clinical Organisms to consider multiple bottles. Local procedures should be followed
feature when taking blood cultures to minimise the risk of
Immunocompromised Cryptococcus contamination with skin flora. When using vacuum
Exposure to rodents or Leptospirosis blood taking systems, care should be taken that blood
contaminated fresh water Hantavirus cultures are inoculated first before filling other blood
Rash Varicella zoster virus tubes. This is to prevent the possibility of bacterial
HSV contamination from blood tubes entering the blood
Measles culture bottles, resulting in a ‘pseudobacteraemia’
Toxic shock Staphylococcus aureus and assigned to the patient.
Streptococcus pyogenes Stool samples should only be sent for micro-
Travel MERS, avian influenza, malaria biology testing when an infective cause is suspected
Animal contact Anthrax, Coxiella for patients with diarrhoea. The Bristol stool scale
can be used to identify diarrhoea stools where types
5–7 indicate diarrhoea. Clostridium difficile should be
time, using the correct technique, the correct volume considered as a cause of hospital acquired infective
and in the correct specimen containers. Lids must be diarrhoea in cardiothoracic centres and requested as a
tightened securely as leakage may mean specimen specific test. Laboratory testing should follow national
rejection, and clinicians and laboratories must ensure testing guidelines to ensure optimal diagnosis. In the
13:43:27
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40
UK this amounts to a combination of tests looking for time as possible to sample processing. Microscopy per-
presence of the C. difficile organism and the presence formed on arrival in the laboratory can provide essen-
of toxin. tial information on the presence of organisms and can
Care should be taken when obtaining respiratory aid antimicrobial management. In patients who have
samples that sputum is collected rather than saliva. had previous cardiac surgery and who develop a deep
Physiotherapists can help with obtaining a good infection or endocarditis where no pathogen is identi-
quality respiratory sample. Any respiratory sample fied, mycobacterial infection should be considered.
obtained in a trap should be transported in a leak-
proof CE marked specimen container. Lower respira- Screening for Resistant Organisms
tory tract samples can be obtained by directed or
Screening for methicillin resistant Staphylococcus
non-directed BAL. Respiratory samples in particular
aureus (MRSA) prior to cardiac surgery and on
must reach the laboratory in a timely manner and
admission to hospital is standard practice in UK
should be processed within 2–3 hours to maximise the
hospitals. Persons carrying MRSA will be offered
chance of culturing respiratory tract organisms.
decolonisation treatment prior to surgery, where
Wound swabs are best obtained after first cleansing
time allows. Some centres also screen for methicillin
the wound. This reduces the risk of contamination of the
sensitive Staphylococcus aureus (MSSA) and offer
sample with therapeutic agents that may be contained
decolonisation prior to cardiac surgery or insertion
within the dressing material. Dry swabs should be mois-
of ventricular assist devices (VAD). Screening for
tened with sterile water (or saline) or transport media.
other resistant organisms is carried out according
Where possible the whole wound should be swabbed
to local and national recommendations but may
using a zigzag movement while rotating the swab.
include vancomycin resistant enterococci (VRE), car-
Fluid from vesicular lesions can be aspirated or
bapenemase producing Enterobacteriaceae (CPE),
swabs used to collect the vesicular fluid and inocu-
multidrug resistant (MDR) Acinetobacter spp.,
lated into viral transport media (VTM).
Enterobacteriaceae producing extended spectrum β-
Urine samples are collected as a midstream sample
lactamases (ESBL) or AmpC β-lactamases. The fre-
after first cleaning the urethral meatus with soap and
quency and nature of who is screened depends on
water or saline. Disinfectants should be avoided as
local resistance patterns, carriage rates, and healthcare
they can irritate the urethral mucosa. However, the
associated infection rates within the local setting and
vast majority of patients in ICU will have a urinary
those of referring hospitals. It is important to note that
catheter in situ. Catheter specimens of urine should
any screening programme should be monitored on a
only be taken where urosepsis is suspected. The cor-
regular basis and action taken when carriage or clin-
rect local procedure should be followed and urine
ical infection rates exceed those expected for a local
sampled through the catheter sampling port.
unit. The implementation of an enhanced screening
If urine samples cannot be examined within 2
programme also depends on what action can be taken
hours then they should be refrigerated until they can
if patients are found to be positive. This may involve
be processed by the laboratory. Urine samples held at
commencement of specific infection control precau-
room temperature will allow overgrowth of bacteria,
tions and/or alteration in prophylactic regimens for
affecting the result. The addition of boric acid to urine
surgery, VAD insertion or transplantation to ensure
containers will preserve the urine sample for longer
that the antibiotic cover at the time of surgery covers
where transport delays exist.
the resistant organism. One very important factor in
being able to action positive screening results within
Surgical Samples critical care units is the availability of side rooms.
Any samples obtained at the time of surgery should be
placed into a sterile pot for onward transportation to the Microscopy and Culture
laboratory. Samples may include native or prosthetic Microscopy and culture of samples continues to be
heart valves, sternal wound biopsies or samples of pus the mainstay of microbial diagnostics. Microscopy
or fluid. These surgical samples are precious, unrepeat- is a quick, useful test indicating the presence of
able specimens and should be notified to the labora- organisms from normally sterile sites, for example
tory ahead of the sample arriving to ensure as short a blood, pericardial fluid or surgical samples, and
13:43:27
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41
also for determining smear positivity in the case of for example aminoglycosides and glycopeptides.
Mycobacterium tuberculosis. Microscopy is less useful Pharmacokinetics and dynamics of various antimi-
at determining the presence of pathogens in samples crobials vary in vivo, for poorly understood reasons,
from non-sterile sites, i.e. the respiratory tract. Urine in many cardiothoracic critical care patients. This is
microscopy can aid in the differentiation between especially true in patients on ECMO where maximum
infection or contamination of the sample by the pres- licensed drug dosing regimens may need to be used
ence of significant numbers of pus cells. Microscopy in drugs with a wide therapeutic window. The alter-
of urine samples is not helpful in catheterised nation of PK/PD is poorly understood in this set of
patients. Culture of the sample is more informative patients but drugs may be sequestered or broken down
than microscopy to enable organism identification as a result of the ECMO circuit. Dosing regimens may
and sensitivity testing. However, this takes time and need to be adjusted based on levels informed by thera-
is influenced by transport times, storage conditions peutic drug monitoring.
and prior antibiotic use. Culture results from non-
sterile sites require a degree of interpretation, taking New Technologies
into account the expected normal flora from the spe-
Speed is an essential factor in the diagnosis of sepsis
cific site. Furthermore, there are some organisms that
and in other acute organ dysfunction states, i.e. severe
by their very nature are difficult to culture, or cannot
respiratory failure, where the appropriate manage-
be cultured or present a danger to laboratory staff.
ment of infection affects outcome. One of the issues is
Thereby other methods of organism identification
that the diagnosis of sepsis can be difficult as clinical
are used.
signs can overlap with other non-infectious systemic
inflammatory states and blood culture results may
Antibiotic Susceptibility Testing take days to complete. New technologies being devel-
Performing antimicrobial sensitivity testing is another oped and introduced into clinical laboratories have
important function of the microbiology laboratory. the potential to speed up microbial diagnosis within
The aim is to inform antimicrobial treatment deci- cardiothoracic units.
sions and detect antimicrobial resistance. Sensitivity
testing requires live organisms and is performed using
a variety of testing methods. Manual disc diffusion Molecular Testing
assays are the mainstay of antimicrobial testing for The development of polymerase chain reaction
most organisms in UK laboratories, alongside gra- (PCR) and other nucleic acid-based amplification
dient diffusion methods (including E-tests). Disc test- technologies (NAATs) over the last 20 years has
ing provides a qualitative measurement, recording the helped to address some of the downsides of culture.
organism as sensitive, intermediate or resistant. More The introduction of such molecular techniques into
qualitative methods that provide a more accurate min- routine clinical microbiology laboratories has revo-
imum inhibitory concentration (MIC) are required lutionised microbial diagnostics. These techniques
for organisms that give borderline results with disc are now used as the primary diagnostic method
diffusion methods or where a more accurate measure for HIV, hepatitis viruses and respiratory viruses.
is required, for example in management of endocar- Amplifying and detecting microbial and genetic
ditis. In addition to manual methods, there are auto- sequences within a prepared clinical sample improves
mated methods commercially available. speed, sensitivity and specificity of microbial testing
and is not so affected by specimen transport times
or prior antibiotic use. The range of organisms that
Therapeutic Drug Monitoring for molecular tests are routinely used for has expanded
Antimicrobials from HIV, hepatitis viruses and respiratory viruses
This is another important function traditionally into bacterial, fungal, parasitic and atypical agents.
carried out in microbiology laboratories but now These techniques are not only used for the diagnosis
often performed in blood science laboratories. Drug of infectious disease but also in the detection of
monitoring is important in drugs with a narrow drug resistant genes. These methods, with the devel-
therapeutic window where it is important to ensure opment of nanotechnology, are also now used for
maximum drug dosing with minimum risk of toxicity, point-of-care testing.
13:43:27
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42
Sequencing organisms detected from non-sterile sites require a

degree of interpretation of the result to consider when
Several sequence based methods have been used to
the organism is a pathogen, when it is normally found
identify microorganisms directly from clinical samples
at that site or when it represents contamination of the
including blood cultures, biopsies and heart valves.
sample. The diagnosis of infection in these circum-
The cost of these tests is high compared with conven-
stances needs to be taken into consideration with the
tional diagnostic methods and they are best used on
clinical picture, inflammatory markers, presence of
samples from normally sterile sites. However, ampli-
fever and localising signs. If the organism is repeatedly
fication and sequencing of 16S rRNA present within
isolated and pus cells are seen on microscopy, the evi-
heart valve samples where no organism has been cul-
dence points to the likelihood of the organism being
tured has changed microbial diagnostics in culture-
pathogenic.
negative endocarditis. Amplification and sequencing
of 18S rRNA is also of value in the identification of
fungal pathogens from samples from normally sterile Liaison with Medical Microbiologists
sites, for example pleural fluid, lung biopsy. These Close liaison on a regular basis between clinical teams
techniques are being researched and developed for and infection specialists is essential to optimise infec-
use in samples from other sites, including the lower tion prevention, diagnosis and management of car-
respiratory tract. diothoracic patients. Such specialist input will not
only optimise appropriate use of antibiotics and infec-
Mass Spectrometry tion control management, but will also assist with
Matrix-assisted laser desorption/ionisation time-of- specimen requesting, provision of laboratory services,
flight mass spectrometry (MALDI TOF MS) is being appropriate use of technologies, and rapid interpret-
used currently for the routine identification of bac- ation and communication of critical results.
terial colonies from positive cultures. Although it
requires culture of the organism and sensitivity testing Learning Points
by conventional means, it provides rapid turnaround • Infections in cardiothoracic intensive care units
of pathogen identification with a minimal amount are common and antimicrobial drugs are used
of labour compared with traditional identification widely and sometimes unnecessarily.
methods. • Correct diagnosis of infections requires careful
physical examination of patients as well as
Microarrays appropriate microbiology testing.
This ‘test-all’ approach allows identification of a large • New technologies being developed and
panel of microbial pathogens from a single sample on introduced into clinical laboratories have the
a single test card within one test run. Cards can be potential to speed up microbial diagnosis within
developed to cover a whole range of relevant patho- cardiothoracic units.
gens based on a syndromic approach. This may prove • Close liaison on a regular basis between clinical
useful in the infection diagnosis of patients with severe teams and infection specialists is essential.
respiratory failure requiring ECMO. The cost of this • Such specialist input will not only optimise
test is comparable to the combined cost of running the appropriate use of antibiotics and infection
PCR tests individually by conventional means, but has control management, but will also assist with
potential clinical benefit in terms of ease of request- specimen requesting, provision of laboratory
ing, sampling and turnaround times. services, appropriate use of technologies, and rapid
interpretation and communication of critical results.
Interpretation of Results
The finding of an organism from a normally sterile site Further Reading
is usually diagnostic of infection with that pathogen. Caliendo AM, Gilbert DN, Ginocchio CC, et al. Better
Some organisms are only ever present when causing tests, better care: improved diagnostics for infectious
an infection, therefore their detection implies infec- diseases. Clinical Infectious Diseases. 2013; 57(Suppl 3):
tion, for example, Mycobacterium tuberculosis. Other S139–S170.
13:43:27
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43
Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis Schweizer ML, Chiang HY, Septimus E, et al. Association
campaign: international guidelines for management of of a bundled intervention with surgical site infections
severe sepsis and septic shock. Intensive Care Medicine. among patients undergoing cardiac, hip or knee
2013; 39: 165–288. surgery. Journal of the American Medical Association.
Kohler P, Kuster SP, Bloemberg G, et al. Healthcare- 2015; 313: 2162–2171.
associated prosthetic heart valve, aortic vascular graft, Tsai D, Lipman J, Roberts JA. Pharmacokinetic/
and disseminated Mycobacterium chimaera infections pharmacodynamic considerations for the optimization
subsequent to open heart surgery. European Heart of antimicrobial delivery in the critcally ill. Current
Journal. 2015; 36: 2745–2753. Opinion in Critical Care. 2015; 21: 412–420.
Liesenfeld O, Lehman L, Hunfeld KP, et al. Molecular Vondracek MI, Sartipy U, Aufwerber E, et al. 16S rDNA
diagnosis of sepsis: new aspects and recent sequencing of valve tissue improves microbiological
developments. European Journal of Microbiology and diagnosis in surgically treated patients with infective
Immunology. 2014; 4: 1–25. endocarditis. Journal of Infection. 2011; 62: 472–478.
Robich MP, Sabik JF, Houghtaling PL, et al. Prolonged Wolk DM, Dunne(Jr) WM. New technologies in clinical
effect of postoperative infectious complications on microbiology. Journal of Clinical Microbiology. 2011;
survival after cardiac surgery. Annals of Thoracic 49(suppl 9): S62–S67.
Surgery. 2015; 99: 1591–1599.
MCQs
True or False 3. Sequencing techniques are best used for samples from
1. Microscopy has been superseded as a method used in normally sterile sites.
bacteriology laboratories. 4. The length of time a sample takes to get to the labora-
2. Molecular testing can only be used for organism tory does not affect the ability to culture pathogens.
identification and not for detection of antimicrobial 5. Finding an organism in a sample always indicates an
resistance. infection.
13:43:27
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44
Section 1 Diagnosis
Radiology for Cardiothoracic Intensivists

Chapter
7 Kristian H Mortensen, Peter A Barry and Deepa Gopalan
Introduction rarely attainable; (c) Distribution of fluid and air in the

pleural space is altered, where a pneumothorax will
Diagnostic imaging of patients in the cardiothoracic
locate to the anterior pleural space and pleural effusions
intensive care unit (ICU) can pose unique challenges.
settle posteriorly on supine CXR, albeit loculations may
Where possible, the patient should be imaged in situ
limit the free movement of pleural collections particu-
using mobile chest X- ray (CXR) and ultrasound,
larly. This may happen when there is longstanding
including transthoracic (TTE) and transoesophageal
pleural disease, prior malignancy or previous surgical
echocardiography (TOE), unless computed tomog-
intervention, and ultrasound or CT will often be pref-
raphy (CT) is specifically required. An outline of the
erable; (d) Forward slumping may obscure apical pul-
advantages and limitations of each imaging modality
monary disease or pneumothorax; (e) Rotation –as
is followed by presentation of the optimal use and
judged by medial clavicles not being equidistant from
escalation of imaging to diagnose specific cardio-
the midline relative to the spinous processes –may
respiratory conditions in the context of this highly
mimic mediastinal disease; and (f) Artefacts such as
specialised setting.
skin folds, hair braids, asymmetrical soft tissues, moni-
toring leads and other radio-opaque equipment over-
Cardiothoracic Imaging Modalities lying the field of interest, may degrade the diagnostic
quality and should be minimised prior to imaging.
Chest X-ray
Chest X-ray (CXR) has a high diagnostic accuracy Ultrasound
for the assessment of the position of lines, tubes and Bedside thoracic ultrasound is predominantly used
drains. When compared with this area and imaging of for assessment of pleural effusions, and to confirm
the lungs and pleural spaces, the accuracy of CXR is CXR findings. Ultrasound may give clues to the nature
less impressive for cardiovascular disease, and hence of a pleural effusion, and has an important role in
CXR should never delay other definitive cardiovas- image-guided thoracic interventions. In experienced
cular imaging in the ICU patient. In established car- hands, ultrasound can also assess for pneumothorax,
diorespiratory disease, serial CXR has an additional but emphysematous lung has the potential to cause
role in the investigation of evolving respiratory misdiagnosis and ultrasound is of limited practical
compromise or non-response to treatment. Despite use. Extensive subcutaneous emphysema and severe
ease of use, daily routine bedside CXR is no longer obesity may limit adequate visualisation of the pleural
encouraged because this does not appear to improve spaces. Echocardiography is invaluable in the assess-
outcomes in ICU patients compared with a directed ment of cardiac valves and chamber function as well
approach. as any pericardial disease, and has been dealt with in a
In the majority of ICU patients, the CXR is acquired dedicated chapter (see Chapter 3).
bedside with the patient in the semi-erect or supine pos-
ition. This has several effects: (a) This gives an antero-
posterior (AP) projection, with apparent enlargement Computed Tomography
of cardiac and mediastinal structures compared to the Thoracic CT is of immense value in the assessment
posteroanterior (PA) projection obtained in the ambu- of the ICU patient, particularly when CXR find-
latory setting; (b) An optimal full-inspiratory view is ings are equivocal or if complex disease processes
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Chapter 7: Radiology for Cardiothoracic Intensivists
are suspected. CT adds valuable information to CXR Acute Aortic Syndrome

findings in up to 70%, changing management in 22%. Aortic dissection, intramural haematoma and pene-
The cross-sectional nature of CT allows more detailed trating ulcer together comprise acute aortic syndrome
interrogation of disease processes and can also provide (Figure 7.1), which is classically encountered in
image guidance for interventions. CT has a particular patients with systemic hypertension or those with pre-
role when cardiac and great vessel disease such as disposing factors such as connective tissue disease.
pulmonary embolus (PE) and acute aortic syndrome However, it can also occur in healthy vessels as a con-
are suspected, but is also a key diagnostic tool for the sequence of iatrogenic injury following intra-arterial
diagnosis of postoperative thoracic collections, pleural catheterisation and intra-aortic balloon pump inser-
or pulmonary sepsis, malignancy, complications of tion. Potentially devastating consequences of aortic
mechanical ventilation, concurrent pulmonary path- dissection include extension into the aortic annulus
ologies, and in the assessment of life support device leading to severe aortic regurgitation, rupture into the
related complications. The diagnostic yield of CT must pericardium causing cardiac tamponade or multiorgan
be weighed against the risks of transporting the ICU ischaemia (coronary, cerebral, spinal, and visceral).
patient to the imaging department. Potentially nephro- CXR has limited value in diagnosing acute aortic
toxic intravenous iodinated contrast medium should syndrome, with a sensitivity of 64% and a specificity
be used with caution, and where potential benefit out- of 86%. Typical features are useful when present, such
weighs risk, attention to pre-emptive renal protection as upper mediastinal widening, double aortic con-
and coordination of the timing of contrast admin- trast and discrepancy between the diameters of the
istration with haemodialysis are helpful. Radiation ascending and descending aorta, displacement of the
constraints are less of an issue in this setting, however trachea and of the left main bronchus, ill definition of
repeated CT imaging should be monitored. the aortopulmonary window, left apical cap, pleural
effusion, haemothorax and widening of the left para-
Imaging for Cardiac Emergencies vertebral sulcus, but their absence cannot exclude
the diagnosis. The CXR may be completely normal
Chest Pain in 11–15%. Echocardiography has immense value in
unstable patients as it is portable, quick and can even
Chest pain in the ICU requires urgent appraisal. The
be used in theatres to facilitate diagnosis. The aortic
differential diagnosis is varied, ranging from life
root, valve and proximal ascending aorta can all be
threatening emergencies to more benign conditions.
assessed with relative ease using echocardiography,
A clue to the aetiology can be gained by focused his-
which also has the ability to document ancillary find-
tory, physical examination and electrocardiogram,
ings such as impairment of ventricular function and
with imaging playing a smaller role.
haemopericardium. A major limitation of the trans
thoracic approach, TTE, is the inability to clearly
Acute Coronary Syndrome visualise beyond the proximal ascending aorta. The
A minority of patients, particularly elderly and females transoesophageal approach, TOE, has a much higher
with risk factors for atherosclerosis such as hyperten- sensitivity of up to 98% for detecting entry tear sites,
sion, chronic renal disease or previous cerebrovascular coronary and great vessel involvement and differential
events, may sustain an acute myocardial infarction flow characteristics in the false lumen. TOE, however,
while being hospitalised for another reason. The first requires sedation and also cannot image the entire
step in its management is expeditious recognition to thoracic aorta.
optimise myocardial salvage and reduce mortality by a Multidetector CT has sensitivity and specificity of
prompt attempt of reperfusion therapy. Non-invasive almost 100%. The high negative predictive value in
imaging such as ECG-gated cardiac CT is not recom- combination with rapid image acquisition and wide
mended as it will not only delay consideration for availability has made CT the investigation of choice in
primary percutaneous coronary intervention (PCI) an acute setting. Triple rule out is a new concept that
or fibrinolysis but also often will be non-diagnostic, can be used in the same study to evaluate the aorta, cor-
particularly in patients with cardiogenic shock, heart onary arteries and pulmonary vasculature. It requires
failure or ventricular tachyarrhythmia. ECG-gating and should ideally be performed using a
13:44:45 45
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46
Figure 7.1 Acute aortic syndrome. Top panel, far left and middle images: ECG-gated CT in a 65 year old male with acute type A aortic
dissection. The aortic root is dilated (black star) with a dissection flap (block black arrow) that extends into neck vessels (thin white arrow)
and the ostium of the left main stem coronary artery (middle image, block white arrow). Top panel, far right image: rupture of descending
thoracic aneurysm with high attenuation blood (white star) around the aorta. Bottom panel: different CT findings of acute aortic syndrome
in different patients. Intramural haematoma with a rim of high attenuation material on the unenhanced CT (far left image); aneurysmal
descending aorta with a dissection flap (middle image, thin black arrow); small penetrating ulcer in the descending thoracic aorta (far right
image, notched arrow).
scanner with 64 slice or higher detector number. The attenuation material representing the incompletely
need for simultaneous opacification of pulmonary and sheared media (cobweb sign) and a wedge of haema-
systemic circulation can be particularly challenging toma (beak sign) that forms to create a space for the
in haemodynamically unstable patients and in some development of the false lumen. Occasionally, circum-
circumstances it is better to do one focused exam- ferential dissection can be complicated by intimo-
ination rather than an all-in-one approach. Initial intimal intussusception (windsock sign). Secondary
unenhanced data are useful to demonstrate crescentic features of aortic dissection include displacement of
foci of high attenuation in the aortic wall due to intra- intimal calcification, delayed enhancement or throm-
mural haematoma or a thrombosed false lumen. On a bosis of the false lumen and complications such as medi-
contrast-enhanced examination, the classical feature astinal and pericardial haematoma and compromise
of dissection is an intimal flap that separates the true from coronary, neck vessel, mesenteric, renal and
lumen that is contiguous with the undissected vessel peripheral vascular involvement. Penetrating ulcers
from the false lumen. The false lumen generally has a are shown as focal crater-like pouching of the aortic
larger cross-sectional area, thin linear strands of low wall with irregular edges in the presence of extensive
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Figure 7.2 Pulmonary oedema and acute respiratory distress syndrome with pneumothorax. Far left image: CXR with pulmonary
oedema in a 60 year old male in the aftermath of acute myocardial infarction. Note the intra-aortic balloon pump (block white arrow) and
Swan–Ganz catheter (thin arrow). Middle image: CXR of a 45 year old male with acute respiratory distress syndrome on extracorporeal
membrane oxygenation (black block arrow). There is a supine, right-sided pneumothorax (white star) with deepened costophrenic sulcus
and contralateral mediastinal shift suggestive of tension pneumothorax. Far right image: axial CT thorax in a different patient with acute
respiratory distress syndrome. Note the gravitational, dependent consolidation in the posterior lung segments with diffuse ground-glass
opacification and fibrosis. There is a left pneumothorax (white star) and surgical emphysema (black arrow head).
aortic atheroma, which is most common in the middle (<12 mmHg); (b) early oedema (12– 15 mmHg)
and distal thirds of the thoracic aorta. with vascular engorgement and peribronchovascu-
CT is the imaging modality of choice for sus- lar cuffing; (c) interstitial oedema (15–25 mmHg)
pected rupture. A peripheral hyperattenuation with progressive blurring of the pulmonary vessels
crescent within the thrombus of an aneurysm on with engorgement of peribronchovascular spaces,
an unenhanced CT is a sign of acute or impending Kerley lines and subpleural effusions; and (d) alveolar
rupture, as is the close apposition of the posterior oedema (> 25 mmHg) with nodular or acinar areas
aortic wall to the spine (draped aorta sign). Rupture of increased opacity that evolve into frank consolida-
into mediastinal, pericardial or pleural spaces tion. CXR can detect the majority of these changes
gives rise to high attenuation haematoma in the and is often adequate, particularly when the mor-
respective anatomical space. Fistulous communica- phological findings are complemented by haemo-
tion with the tracheobronchial tree or oesophagus dynamic data. CT is reserved for cases where there is
is a recognised complication. CT may not show the a need to distinguish hydrostatic oedema from other
communication, but development of haemoptysis/ causes. The combination of upper lobe predominant
haematemesis and new onset of pulmonary haem- ground-glass opacification with a central distribution
orrhage/ consolidation should raise the clinical and central airspace consolidation favours hydro-
suspicion. static oedema. Conversely, ARDS classically gives
rise to a gravitational anteroposterior density gra-
Pulmonary Oedema dient within the lung due to dense consolidation in
Pulmonary oedema may be hydrostatic as seen in car- the dependent region and normal or hyperexpanded
diac disease, renal failure or overhydration. Alterna lung in the non-dependent regions, which merge into
tively, it may be non-cardiogenic due to increased a background of diffuse ground-glass opacification.
permeability oedema as encountered in acute Additionally, ARDS persists for days to weeks, does
respiratory distress syndrome (ARDS) (Figure 7.2). not respond to diuretic therapy and may progress to a
Differentiating cardiogenic and non-cardiogenic pul- reticular pattern due to secondary fibrosis.
monary oedema is arduous, and most optimally would
require measurement of pulmonary capillary wedge Cardiogenic Shock
pressure. Image findings in hydrostatic pulmonary Cardiogenic shock is characterised by systemic hypoten-
oedema depend on the degree of elevation of the pul- sion and tissue hypoxia secondary to decreased cardiac
monary capillary wedge pressure: (a) no abnormality output. Diagnostic evaluation should be carried out in
13:44:45 47
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conjunction with resuscitative efforts. Ultrasonography Right Ventricular Failure

and TTE are essential bedside imaging modalities, The aetiology varies from worsening of compensated
which allow rapid assessment of multiple organ systems right ventricular failure, frequently seen in chronic
including cardiac chambers for biventricular function, left-sided heart or pre-existing lung disease such as
proximal aorta for aortic dissection, pleural and peri- emphysema, to acute right ventricular failure in mas-
cardial spaces for effusions, and the abdominal cavity sive pulmonary embolus, right- sided myocardial
for peritoneal fluid and organ appearances. A port- infarction, ARDS or sepsis (Figure 7.4). Pulmonary
able CXR is useful for the exclusion of pneumothorax, artery catheterisation provides reliable and con-
whilst targeted imaging such as thoracic CT should be tinuous monitoring of haemodynamic parameters
considered in patients in whom the aetiology of the cir- whilst echocardiography allows for bedside evaluation
culatory failure remains unclear despite initial bedside of cardiac function although estimates of RV systolic
imaging. Coronary angiography should not be delayed and pulmonary artery pressure can be inaccurate in
in patients with suspected myocardial infarction who patients with chronic lung disease and those under-
might be candidates for revascularisation. going IPPV. CXR is of limited value and can dem-
onstrate generic features such as cardiomegaly and
Pericardial Tamponade
proximal pulmonary artery dilatation. It can be useful
Tamponade can occur due to collection of fluid, for tracking of lung parenchymal changes like atelec-
blood, pus, air or soft tissue within the pericardial tasis or consolidation and pleural effusions, and for
space (Figure 7.3). Although challenging, it is fore- the assessment of lines, tubes and drains. CT can be
most a clinical diagnosis and must be considered in all more useful in detailing this pathology.
patients with unexplained cardiogenic shock or pulse-
less electric activity. TTE is the most appropriate ini- Pulmonary Embolus
tial imaging modality as it facilitates assessment of the CT pulmonary angiography is the imaging modality
haemodynamic impact and may guide diagnostic and of choice in suspected PE. With optimisation of
therapeutic pericardiocentesis. Progressively enlar- contrast enhancement (Hounsfield unit >200 in the
ging cardiac silhouette resulting in a globular feature- main pulmonary artery) and minimisation of motion
less water-bottle appearance is a characteristic feature artefact, the high spatial resolution of modern CT
on serial CXRs. However, tamponade due to pneu- scanners allows for the detection of emboli down to
mopericardium can cause reduction in the size of the 2–3 mm. Acute emboli can occlude the entire lumen,
cardiac silhouette with sharp outlining of the pericar- or form central filling defects surrounded by a rim
dium by radiolucent air. CT is not routinely indicated of contrast, causing the ‘polo mint’ sign on images
for the diagnosis and should be reserved for cases perpendicular to the long axis of a vessel and ‘railway
where there is diagnostic uncertainty. The attenuation track’ sign on longitudinal images. When periph-
value of the collection on a precontrast scan can give eral, thrombi form an acute angle to the vessel wall
a clue to its nature, with haemopericardium typically as opposed to chronic thrombus that is eccentric with
being of higher attenuation than simple fluid. Imaging obtuse angle to the fibrosed arterial wall. The pres-
features such as compression of the cardiac chambers ence of stenosis, intravascular webs, bronchial collat-
and coronary sinus, straightening of the right heart erals and mosaic perfusion patterns implies chronic
border, interventricular septal bowing, distension of thromboembolic disease. Peripheral wedge- shaped
the systemic veins and reflux of contrast medium into areas of hyperattenuation representing infarcts can
the azygos vein may be seen even on non-ECG gated be seen in acute as well as chronic thromboembolic
CT. Although the addition of gating will improve disease. Obstruction of more than 30% of the pul-
the anatomical and functional delineation, the need monary circulation can raise the pulmonary vascular
for prompt treatment should override any poten- resistance sufficiently to produce significant pul-
tial delays in image acquisition. Percutaneous drain- monary hypertension. CT signs of RV strain include a
age should be performed using image guidance, and right-to-left ventricular diameter ratio >1.0, leftwards
echocardiography, fluoroscopy or CT have all been septal bowing, abrupt increase in size of the azygos
shown to be successful, with the relative use of each vein, widening of the vascular pedicle, and reflux of
technique much depending on the institutional and contrast medium into a distended inferior vena cava
individual preferences. and hepatic veins.
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Figure 7.3 Pericardial tamponade. Top panel: pneumopericardium (left image, black arrows) and globular cardiac silhouette secondary to
pericardial effusion (right image) on CXR. Lower panel: pericardial collections on CT. Haematoma (left image, black star) with compression
of the underlying cardiac chambers, and ventricular assist device catheters in situ. Circumferential pericardial thickening and enhancement
(right image, block white arrow) secondary to a purulent collection (white star) with an enhancing left pleural collection (thin white arrow).
Complications of Cardiac Surgery tamponade and left ventricular outflow tract obstruc-
The use of cardiopulmonary bypass during cardiac sur- tion are some potential culprits. In addition to haemo-
gery results in a distinct group of postoperative com- dynamic assessment and ECG, TTE is often the most
plications. Unexplained hypotension, tachycardia and useful initial imaging modality. CXR excludes non-
pulmonary oedema should raise the suspicion of postcardiac complications such as pneumothorax, haemo-
surgical cardiac dysfunction. Coronary artery graft thorax, pneumonia, atelectasis, pleural effusions and
occlusion, prosthetic valve malfunction, pericardial diaphragmatic injury, and malposition of lines and
13:44:45 49
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RV
Figure 7.4 Right ventricular failure. Top panel: massive, acute pulmonary emboli (block white arrows) with right ventricular (RV)
enlargement alongside interventricular septal bowing (thin white arrow) and a pulmonary infarction (notched arrow). Bottom panel: catheter
angiography with thrombolysis for acute pulmonary embolus (left image, white arrow) and another patient with idiopathic pulmonary
arterial hypertension with right-sided cardiac chamber dilatation and right ventricular hypertrophy (right image). The latter patient had
acute decompensation with development of pneumonia in the right lower lobe complicated by formation of segmental pulmonary artery
pseudo-aneurysm (right image, black block arrow).
tubes. Neurological complications such as ischaemic be used with caution. Some abdominal conditions
cardiovascular insults or intracranial haemorrhage such as cholecystitis can be diagnosed by ultrasound,
will often require an unenhanced CT for confirmation. whilst persistent elevation of inflammatory markers
Bowel ischaemia can be precipitated by atheroembo- and metabolic disturbances that require exclusion of
lism, intracardiac thrombus, atrial fibrillation, acute intra-abdominal sepsis will require a CT for more
aortic syndrome and tissue hypoperfusion. Arterial comprehensive assessment.
and portal venous phase CT of the abdomen and
pelvis is often needed but since up to 30% of patients Respiratory Emergencies
who have undergone cardiac surgery can suffer from CXR is the first line imaging modality, in the setting of
acute renal injury, iodinated contrast medium should both de novo and persistent or worsening oxygenation
13:44:45
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51
levels. CT offers superior accuracy for the underlying emphysema hinders the ability to diagnose under-
cause, but serial bedside radiography may in many lying pneumothorax.
instances be sufficient.
Pleural Effusion
Desaturation Associated with Pleural Fluid in the pleural space is exceedingly common in
Abnormalities the critically ill, and may be a transudate, exudate,
pus, blood or chyle. Blunting of the costophrenic
Pneumothorax angles is a sine qua non on the erect or semi-erect
Pneumothoraces are common in the ICU but their CXR, and there may be associated volume loss of the
recognition is lacking with up to 30% missed on adjacent lung. When the effusion accumulates in the
CXR. Even small pneumothoraces are important subpulmonary space, the findings include: (a) a seem-
because they may rapidly become clinically sig- ingly elevated hemidiaphragm with a lateral shift of
nificant during positive pressure ventilation. The the diaphragmatic apex and blunted costophrenic
volume of the pneumothorax dictates the associated angle; and (b) increased density below the diaphragm
pulmonary changes, which range from small areas with no bronchovascular markings and a gastric air
of atelectasis to extensive collapse. Imaging of ten- bubble that is situated well below the apparent dia-
sion pneumothorax, with ensuing circulatory com- phragm. On supine CXR, the costophrenic angle may
promise, must not delay emergency decompression. not be blunted but there may be: (a) a hazy ‘veil-like’
If CXR has been obtained, signs of tension include opacity, with bronchovascular markings visible, due
extensive lucency of the hemithorax with contralat- to dependent layering of the fluid in the paraverte-
eral mediastinal shift and ipsilateral diaphragmatic bral gutters and posterior pleural space; and (b) an
flattening. apical cap (when this is most dependent) and fis-
Stereotypical CXR signs of pneumothorax include sural thickening. The presence of gas locules and
a medial position of the visceral pleural line, with loculations should raise the possibility of empyema
absent bronchovascular markings lateral to this line. (Figure 7.5). CT better characterises the complex
The air typically collects at the apex when erect or pleural collection, depicting pleural thickening,
semi-erect but the movement of air may be impeded enhancement and separation in empyema, and can
by loculations. The supine CXR is more challen- differentiate hypodense fluid and pus from hyper-
ging, with signs of pneumothorax including the fol- dense blood, especially important after recent sur-
lowing: (a) a deep, sometimes tongue-like, lateral gery or trauma. The need for sampling is governed by
costophrenic sulcus; (b) sharp demarcation of the clinical presentation.
diaphragm or cardiomediastinal silhouette; (c) gas On the erect CXR, blunting of a lateral costo-
outlining the costophrenic or cardiophrenic sulci; phrenic angle can be seen with as little as 200 ml but
and (d) hyperlucent right upper quadrant. Skinfolds may be absent with as much as 500 ml. The semi-
can be mistaken for a pneumothorax, but should erect CXR is less sensitive to pleural fluid and may
be differentiated by noting continuation of the line miss even moderate effusions. Bedside ultrasound
beyond the thoracic cavity and the presence of vas- is very useful with the pleural fluid demarcated by
cular markings beyond the apparent line. Previous either the echogenic visceral pleura or by lung that
imaging may show the presence of a bulla in emphy- may be hyperechoic when there is atelectasis, collapse
sematous patients. A lateral decubitus, horizontal or consolidation. The fluid can have internal echoes,
shoot-through or expiratory CXR may help clarify layering and septations depending on its nature and
the presence of a suspected pneumothorax when duration. Even though some guidance can be taken
there is doubt. However, the sensitivity of CT and its from ultrasound appearances (e.g. most transudates
ability to assess the underlying cause make it the diag- are without internal echoes), ultrasound appear-
nostic modality of choice in these situations. CT is ances should not be taken as specific to the nature of
also more sensitive to pneumomediastinum, which in the fluid. Ultrasound can also aid sampling of pleural
the ventilated patient may be due to barotrauma, and fluid and drain insertion, improving the safety of
CT may be preferred when extensive subcutaneous these procedures.
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Figure 7.5 Empyema, lung abscess and sepsis. Top panel: CXR and CT demonstrate a loculated left pleural collection with (right image,
white star) locules of free air secondary to empyema (right image, thin white arrow). Bottom panel: CXR of a cavitating lung abscess (left
image, block black arrow) and left lower lobe collapse with a tiny effusion in an immunocompromised patient. Another profoundly septic
patient with recent aortic valve replacement has sternal dehiscence due to osteomyelitis shown on CT (right image, block white arrow).
(A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)
Desaturation Associated with Pulmonary involvement. Volume loss is the most common find-
ing on CXR in the ICU setting, often present as sub-
Abnormality segmental linear atelectasis in the dependent lower
lobes, and resolves spontaneously. CXR findings in
Atelectasis and Collapse
collapse and atelectasis will depend on the extent of
Atelectasis and collapse represent pulmonary volume volume loss but classically are those of increased opa-
loss, with the latter implying more extensive, lobar city with (a) loss of contour of the diaphragm, heart
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or mediastinum, (b) shift of pulmonary fissures, hilar more patchy involvement but also limited to a lobe;
points, mediastinal structures or hemidiaphragm, and (c) interstitial pneumonia, with initially more
(c) bronchovascular crowding or (d) hyperinflation linear opacities that can have a nodular appearance.
of non-affected lung. With smaller atelectasis, for Appearances similar to infective consolidation can
example due to scarring or a patchy area of insuffi- appear with fluid, blood, aspirate or tissue filling the
cient surfactant with alveolar collapse, a linear opa- alveoli, and correlation with markers of sepsis and
city with little volume loss is more typical. clinical presentation are essential. Classically, the
The distinction between obstructive atelectasis, consolidation caused by pneumonia will take days to
due to endobronchial obstruction or compression, improve whereas for instance that due to pulmonary
and passive atelectasis, caused by external compres- oedema resolves within hours.
sion of alveoli, is important. In the ventilated patient, In many cases of pneumonia there will be predis-
endobronchial obstruction from mucus plugging posing lung disease, with an acute or chronic insult
is a common cause of acute segmental atelectasis or causing hypoxia. It can be extremely helpful to com-
lobar collapse, which responds well to endobronchial pare with prior CXRs and to look for underlying
intervention. Other causes of obstructive atelectasis pathology within areas of non-consolidated lung.
include aspiration, inhaled foreign body, blood clots, Common associations of acute pneumonic exac-
endotracheal tube malposition and bronchial neo- erbations on chronic lung disease include emphy-
plasm. Passive atelectasis or collapse when air is forced sema, bronchiectasis and interstitial lung disease,
out of the alveoli will necessitate therapeutic measures which in the majority of cases will be recognised
addressing the underlying cause. Air bronchograms by CT or CXR. Disease progression can be rapid,
favour an obstructive over a passive process and indi- and early CT can help diagnose occult disease in
cate higher likelihood of successful inflation following patients with persistent sepsis of unknown origin,
bronchoscopy. The differentiation from pneumonia with as many as 40% of CXRs in immunocom-
may be difficult, especially on the supine CXR where promised patients not demonstrating pneumonic
volume loss is more difficult to assess. Here CT may consolidation. CT also has an important role when
help by showing relatively reduced enhancement in there is a suspicion of pneumonia related compli-
infective consolidation. cations such as cavitation, empyema, abscess for-
mation or bronchopleural fistulation. Mediastinal
Pneumonia collections are also a differential diagnosis in septic
Pneumonia is common in the ICU with aspiration patients, especially in the postoperative patient,
and mechanical ventilation contributing as risk fac- and CT should be utilised when findings are incon-
tors. The radiographic diagnosis of pneumonia can sistent with pneumonia.
be particularly challenging in the ventilated patient,
with as many as 62% with clinical diagnosis of pneu- Aspiration
monia not recognised from CXR. Consolidation is Risk factors include intubation, impaired cough
the key radiographic finding, occurring when the or gag reflex, sedation and enteric tube feeding.
airspaces have become filled with inflammatory Aspiration in the recumbent position most com-
material. The vessels are obscured and air broncho- monly affects the upper lobes (posterior segment)
grams appear due to increased visibility of large and lower lobes (superior segment). A rapid onset of
airways. The increased density of the involved lung ill-defined areas of ground-glass opacity, consolida-
leads to effacement of the contours of the struc- tion or nodularity represents acute airway plugging
tures that it abuts (the diaphragm, mediastinum and and surrounding inflammatory response, and can
heart), which aids in localising consolidation to spe- be seen on CXR and CT. The imaging findings often
cific lobes. In addition, a straight line indicates con- increase over the initial 24–48 hours and diminish
solidation limited by a fissure. Pleural effusions are thereafter. Progression or persistence indicates the
common ancillary findings, and in the septic patient development of complications. CT may depict the
the possibility of empyema must always be consid- dependent changes in more detail but its main role
ered. Pneumonic consolidation may take the form is demonstration of suspected cavitation and abscess
of: (a) lobar pneumonia, classically with diffuse conformation, which are increased in patients who
solidation of a lobe; (b) bronchopneumonia, with aspirate non-sterile stomach contents.
13:44:45 53
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Acute Respiratory Distress Syndrome 24– 48 hours whereafter they start to resolve over
ARDS is a severe form of acute lung injury, where the following 7–10 days. Classically, contusions are
increased capillary permeability causes influx of fluid ill-defined patchy areas of ground-glass opacity and
and protein into the interstitium and alveoli. ARDS consolidation that do not adhere to the bronchopul-
may be caused by a whole range of both intratho- monary segmental anatomy and often have subpleural
racic or extrathoracic disease. The radiological diag- sparing. If resolution within the expected timeframe
nosis of ARDS is, in the appropriate clinical context, does not occur, then compounding diseases such as
made based on bilateral pulmonary opacities in the pneumonitis from fat embolism, aspiration, ARDS
absence of heart failure. In its classical form, ARDS and pneumonia need to be entertained. Lacerations
follows a triphasic pattern: (a) exudative phase (day 1– are areas where the lung parenchyma has lost its
7), with an initially normal CXR followed by patchy, integrity, which may appear as focal abnormalities on
symmetrical bilateral consolidation; (b) proliferative imaging that may be filled with air or blood (pneuma-
phase (day 7–14), when the initial changes persist but tocele or haematoceles, respectively). In the patient
may take on a more coarse and linear pattern; and with deteriorating oxygenation after initial stabilisa-
(c) fibrotic phase (>15 days), when the changes begin tion, undiagnosed haemothorax or pneumothorax
to resolve and may completely resolve or leave the will need to be excluded using bedside CXR initially.
lungs fibrotic. In the exudative phase, appearances are Tracheobronchial tears and bronchopleural fistulation
similar to pulmonary oedema but ARDS is indicated (BPF) are often difficult to detect on initial imaging,
when there is a more peripheral and dependent distri- and should be suspected with worsening pneumo-
bution with a lack of response to diuretics. In addition, thorax, pneumomediastinum or pleural effusions.
the patient with ARDS without prior cardiac disease Most BPFs are, however, not traumatic but result from
will have normal cardiac size with absence of upper surgical intervention (pneumonectomy) or necrotis-
lobe diversion, septal lines and pleural effusions. CT ing pneumonia, with other causes including neo-
may aid the characterisation of ARDS, showing an plasia and radiotherapy. Radiological findings of BPF
anterior-posterior gradient, heterogeneous mixture include a drop in the air-fluid level exceeding 2 cm
of ground-glass opacity and consolidation, and bron- during the postoperative period or the reappearance
chial dilation within affected areas. Decreased lung of an air-fluid level in a patient who has undergone
compliance increases the risk of complications of pneumonectomy (Figure 7.6).
the required positive pressure ventilation, including Postoperative lung torsion (Figure 7.7) can cause
pneumothorax, interstitial emphysema and pneumo- rapid clinical deterioration and is due to rotation of
mediastinum. This may be surveyed with serial CXRs a lobe or the whole lung around the hilar structures
but when there is extensive disease, pneumothoraces resulting in compromise of the airways, vasculature
may be extremely difficult to diagnose without the and the lymphatic drainage. Rapid opacification of the
use of CT. lung or unusual position of a collapsed lobe on a radio-
graph should raise the suspicion. CT is often required
Desaturation Associated with Trauma and Surgery prior to lung salvage and demonstrates obliteration
of the proximal pulmonary artery and accompanying
CT diagnoses 20% more injuries than CXR, in par-
bronchus with poorly enhancing consolidation,
ticular pulmonary contusions, aortic injuries and
ground-glass attenuation, interlobular septal thicken-
osseous trauma. Many CXR-detected injuries are also
ing and intralobular linear attenuation with bulging
upgraded in severity by CT. Nevertheless, bedside
of the neofissure. Traumatic phrenic nerve injury and
CXR maintains an important role for the immediate
diaphragmatic rupture may be concealed by positive
diagnosis of large pneumothoraces, flail chest, and
pressure ventilation and may also need fluoroscopy or
malpositioned lines and tubes.
CT for confirmation.
Pulmonary contusions are areas of alveolar haem-
orrhage that occur in intact lung parenchyma, and are
most commonly seen in blunt trauma when tearing- Conclusion
shearing forces have been applied. Contusions may The highly specialised setting of the cardiothoracic
become apparent any time from the time of injury intensive care unit demands detailed knowledge of
until 6 hours after, and can progress during the initial the natural history and treatment complications of
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Figure 7.6 Bronchopleural fistula and abdominal ischaemia. Top panel: CXR performed on day 19 (left image) and day 23 (right image)
after left pneumonectomy with the drop in the air-fluid level highly suspicious for bronchopleural fistula; this would require CT confirmation.
Bottom panel: elderly patient with septic shock and an intra-aortic balloon pump (left image, notched arrow) in the distal descending
thoracic aorta. There is multiorgan ischaemia as evidenced by heterogeneous liver attenuation (right image, white star), thickened stomach
with intramural gas (right image, thin white arrows). Also note small bowel dilatation on the CT scout view (left image).
particular disease processes. The timely recognition of

specific imaging findings necessitates close collabor-
Learning Points
ation between specialised radiologists and clinicians. • Systematic CXR evaluation is essential taking into
Serial imaging must, where available, be reviewed in account the positioning of the patient and mode
light of ever changing clinical circumstances. In cer- of acquisition at the time of imaging.
tain life threatening emergencies, lack of imaging • CXR should be undertaken to help answer a
should not delay prompt intervention. specific clinical question; routine CXR, as a part
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Figure 7.7 Pulmonary torsion.

Thoracic CT on mediastinal (left image) and lung (right image) windows in a patient with severe deterioration 2 days following right
lobectomy. There is tapered obliteration of the proximal pulmonary artery and accompanying bronchus with poorly enhancing
consolidation (left image, white star), diffuse ground-glass attenuation (right image) and interlobular septal thickening (right image, thin
black arrow), which are all features in keeping with ischaemia and oedema due to lobar torsion.
of the daily assessment of patients in the intensive Ayres J, Gleeson F. Imaging of the pleura. Seminars
care unit, does not improve outcomes. in Respiratory and Critical Care Medicine. 2010;
• Review of previous CXRs provides important 31: 674–688.
diagnostic clues to the nature of thoracic disease Bentz MR, Primack SL. Intensive care unit imaging. Clinics
and helps identify causes for acute clinical in Chest Medicine. 2015; 36: 219–234, viii.
deteriorations by demonstrating the evolution Eisenhuber E, Schaefer-Prokop CM, Prosch H, Schima
over time. W. Bedside chest radiography. Respiratory Care. 2012;
57: 427–443.
• Bedside echocardiography should be the first
line imaging for assessment of cardiac function, Franquet T, Gimenez A, Roson N, et al. Aspiration
diseases: findings, pitfalls, and differential diagnosis.
cardiac valves and the pericardium.
Radiographics. 2000; 20: 673–685.
• CT should be reserved as a problem-solving tool,
McMahon MA, Squirrell CA. Multidetector CT of aortic
to be used only when the diagnosis is unclear
dissection: a pictorial review. Radiographics. 2010;
even after careful review of portable imaging. 30: 445–460.
Oikonomou A, Prassopoulos P. CT imaging of blunt chest
Further Reading trauma. Insights into Imaging. 2011; 2: 281–295.
Amorosa JK, Bramwit MP, Mohammed TL, et al. ACR Sheard S, Rao P, Devaraj A. Imaging of acute respiratory
appropriateness criteria routine chest radiographs in distress syndrome. Respiratory Care. 2012; 57: 607–612.
intensive care unit patients. Journal of the American Trotman-Dickenson B. Radiology in the intensive care
College of Radiology. 2013; 10: 170–174. unit (Part I). Journal of Intensive Care Medicine. 2003;
18: 198–210.
MCQs
1. Signs of right lower lobe collapse on CXR include: (c) High position of the left hilum
(a) Inability to see the line of the right hemidiaphragm (d) Decreased transradiance of the right upper lobe
(b) Inability to see the line of the right heart border (e) High position of the right horizontal fissure
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2. Alveolar opacities in hydrostatic pulmonary oedema 4. CT pulmonary angiographic features of acute PE

are seen on CXR: include:
(a) With a pulmonary capillary wedge pressure (a) Central vascular filling defect
<25 mmHg (b) Eccentric vascular thrombus
(b) Immediately with an increase in intracapillary (c) Intravascular webs
pressure
(d) Pulmonary stenosis
(c) Prior to the development of pleural effusions
(e) Thrombus forms obtuse angle with the vessel wall
(d) After blurring of the pulmonary vasculature
5. Echocardiographic indicators of haemodynamic com-
(e) with a distinctive appearance from ARDS promise secondary to pericardial tamponade include:
3. A peripheral crescent of high attenuation in the aortic (a) Inspiratory collapse of right-sided chambers
wall in unenhanced CT is seen with the following:
(b) Early-systolic right ventricular inversion
(a) Penetrating ulcer
(c) Rightward septal shift
(b) Intramural haematoma
(d) Reciprocal respiratory variation on Doppler
(c) Aortic aneurysm less than 6 cm transvalvular flow
(d) Atherosclerotic plaque (e) Increase in inferior vena caval diameter during
(e) Aortic aneurysm greater than 6 cm inspiration
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Section 2 Practical Procedures
Airway Management in Cardiothoracic

Chapter
8 Intensive Care: Intubation and

Tracheostomy
Martin John and Christiana Burt
The ability to safely secure and manage a definitive Patients who are breathing unsupported or receiv-
airway on the cardiothoracic intensive care unit is an ing non-invasive ventilation may require intubation
essential and challenging skill. Patients are frequently for a number of reasons (Table 8.1).
haemodynamically compromised with reduced car-
diorespiratory reserve, resulting in poor tolerance of Airway Assessment
suboptimal ventilation.
When planning any intubation, it is important to per-
Important airway competencies within cardiotho-
form an initial airway assessment to gauge whether
racic intensive care include endotracheal intubation
there may be any potential difficulties with facemask
and tracheostomy forming techniques, as well as a
ventilation or laryngoscopy. A key finding from the
good working knowledge of how to rescue the airway
4th National Audit Project on major airway events in
should initial attempts fail.
the UK found that poor airway assessment contrib-
uted to poor airway outcomes. The degree of harm
Tracheal Intubation from airway incidents was also found to be highest in
The presence of a cuffed tube within the trachea repre- intensive care patients.
sents a secure airway, providing protection from aspi- Recognised predictors of difficult intubation are
ration and facilitating positive pressure ventilation. listed in Table 8.2. An absence of these signs how-
Endotracheal tubes are made from polyvinyl chloride ever does not guarantee straightforward airway
and are sized based on their internal diameter in mil- management.
limetres. Since the internal diameter is inversely pro-
portional to airflow resistance, it is appropriate to use Performing Endotracheal Intubation
the largest size that can be easily accommodated (usu-
The intubating environment on the intensive care unit
ally 8–9 mm for males and 7–8 mm for females).
can be very different from that of the elective operat-
Many patients following cardiac surgery already
ing room. Critically ill patients have less physiologi-
have an endotracheal tube in place when admitted
cal reserve and often require intubation urgently to
to the critical care unit. In these patients a period of
address cardiorespiratory collapse. They may not be
haemodynamic stability may be required before prep-
fasted and often experience delayed gastric emptying,
arations are made for discontinuation of sedation and
so a rapid sequence induction with cricoid pressure is
extubation. It is important to document the endotra-
often performed.
cheal tube position, laryngoscopic grade and whether
there were any difficulties with facemask ventilation
and/or intubation following induction. Preparation
In contrast, the postoperative management of Prior to intubation, it is necessary to prepare the
patients following thoracic surgery tends to focus on patient, drugs, equipment and intubating team. Roles
early extubation and the avoidance of positive pres- should be applied to appropriately skilled personnel
sure mechanical ventilation where possible. This is and a backup plan for a failed intubation should be
to avoid positive pressure stress on suture and staple in place. Essential equipment required for emergency
sites, which may increase the risk of postoperative intubation, along with rescue equipment in case of
complications including persistent air leaks. difficulty, should be immediately available in the
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Section 2: Practical Procedures
Table 8.1 Indications for tracheal intubation on the critical Equipment

care unit
Basic airway equipment includes: a self-inflating bag,
Hypoxia gum-elastic bougie, oropharyngeal airway, function-
Hypercarbia ing laryngoscope (with a spare in case of failure) and
Reduced conscious level at least two options of appropriately sized endotra-
Increased work of breathing cheal tubes. A supraglottic airway device (laryngeal
Cardiac arrest mask airway, LMA) should also be present in case
Airway obstruction of intubation difficulty, in order to assist with rescue
To facilitate transfer
oxygenation. A suitable device for emergency crico-
thyrotomy should also be available in case of failure to
intubate or oxygenate.
Table 8.2 Predictors of difficult intubation It is necessary to be able to tilt the patient’s bed
in a head-down position in case of regurgitation dur-
Receding chin
ing airway manipulation and to have working suction
Short neck
available. It is also prudent to ensure the ventilator
Thick neck to be used after intubation is fully operational and
Limited neck extension/flexion attached to a reliable oxygen source.
Long upper incisors Occasionally it may be necessary to site a double-
Prominent overbite lumen endotracheal tube rather than a single-lumen
Inability to extend mandibular incisors anterior to the maxillary tube, either to facilitate protection of one lung from
incisors soiling by secretions or blood from the other lung, or
Less than 3 cm interincisor distance to enable differential ventilation of the lungs. Double-
High arched palate lumen tube placement requires additional experience
Less than 3 finger breadth thyromental distance and specific training.
Mallampati score greater than II
Non-compliant mandibular space
Drugs
Adapted from American Society of Anesthesiologists Task Force
Rapid sequence induction involves the administra-
on Management of the Difficult Airway (2013). tion of a predetermined dose of intravenous induc-
tion agent followed immediately by a neuromuscular
blocking drug to achieve rapid loss of consciousness
intensive care unit and moved to the patient’s bed- and optimal intubating conditions with minimal
space. A ‘difficult airway’ trolley containing basic and patient apnoea time.
advanced equipment is an ideal way to organise this. The haemodynamic side effects of the common
induction agents at dosages used in anaesthetic prac-
Patient tice are such that their administration in critically
Critically ill patients requiring intubation should have ill patients can cause catastrophic cardiovascular
standard monitoring (non-invasive blood pressure, collapse. To reduce the amount of induction agent
electrocardiography, pulse oximetry) and working needed, operators often coadminister opioids and
intravenous access as a minimum. Capnography to benzodiazepines. Despite coinduction, vasopressors
confirm correct tube position after intubation should are still frequently needed following induction and
be immediately available. should be immediately available.
Head position should be gently manipulated (if it Suxamethonium has been the traditional neuro-
is safe to do so) into the ‘sniffing the morning air posi- muscular blocking agent used to achieve paralysis due
tion’ which includes a mild amount of cervical flex- to its speed of onset and offset. Rocuronium is now an
ion (a pillow is usually necessary behind the head to alternative option, since the recently developed sug-
provide this) and mild atlanto-occipital extension in ammadex allows immediate block reversal in case of
order to optimise direct laryngoscopic view. In obese emergency.
patients extra pillows may be necessary behind the The choice of drugs used should be tailored to the
shoulders in order to allow atlanto-occipital extension. individual critical care patient based on an assessment
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Chapter 8: Airway Management: Intubation and Tracheostomy
Table 8.3 Commonly used intubating drugs preoxygenation, cricoid pressure, anaesthetic induc-

tion, paralysis, laryngoscopy and confirmed endotra-
Drug Comments
cheal intubation.
Thiopentone Fastest speed of onset
Cardiovascular suppression Preoxygenation
Potential harm from extravasation Preoxygenation describes the process of replac-
Propofol Rapid speed of onset ing nitrogen with oxygen in the functional residual
Suppresses laryngeal reflexes capacity (FRC) of the lungs to maximise oxygen
Cardiovascular suppression stores. This allows for a longer apnoeic time to
Ketamine Slower onset time
secure the airway before desaturation occurs, and
should be performed where possible. Effective
Cardiovascular stability
preoxygenation is performed by encouraging the
Bronchodilation
patient to take tidal volume breaths of 100% oxygen
Etomidate Rapid speed of onset through a tight fitting mask (to prevent entrainment
Cardiovascular stability of air) at flows above 10 l (to minimise rebreathing)
Possible adrenal suppression for 3–5 minutes. Since FRC is lower in the supine
Midazolam Slower onset time position, adopting a head-up position can improve
Prolonged duration of action oxygen storage capacity. An expired oxygen concen-
Reduces anaesthetic dose requirements tration of 90% signifies effective preoxygenation.
Opioids Unreliable amnesic These ideal conditions for preoxygenation are not
always possible, particularly in patients requiring
Limits sympathetic response to intubation
intubation for respiratory failure who are deterio-
Reduces anaesthetic dose requirements
rating despite non-invasive respiratory support, or
Suxamethonium Rapid onset and offset of paralysis
who are not able to cooperate with instructions. In
Hyperkalaemia these patients a careful attempt at preoxygenation
Risk of malignant hyperthermia can often be made, but care must be taken not to
Rocuronium Rapid onset of neuromuscular block cause stomach inflation, which increases the risk of
Rapid reversal with sugammadex regurgitation and aspiration.
Cricoid
of aspiration risk, physiological reserve and indication Cricoid pressure is a manoeuvre intended to reduce
for intubation (Table 8.3). the risk of aspiration during induction. The circum-
ferential cricoid cartilage is the most inferior laryngeal
Team structure and can be pressed against the body of the
Clear roles matched to the skillset within the team fifth cervical vertebrae to compress the oesophageal
need to be allocated prior to induction. The team lumen. The thumb and index finger are placed either
leader is responsible for the overall running of the side of the cartilage and a posterior force of 10 N is
intubating process and ideally should not be per- applied before induction, which is increased to 30 N
forming any other tasks. The first intubator performs following loss of consciousness. The assistant applying
preoxygenation, laryngoscopy and intubation, with a cricoid pressure needs to be experienced since incor-
second intubator on standby in case of failure. One rect technique can result in airway obstruction and a
team member is responsible for administering drugs poor view on laryngoscopy.
and another should be competent at performing cri-
coid pressure. Laryngoscopy
Laryngoscopy is most commonly performed with a
curved Macintosh laryngoscope blade (sizes 3–5) to
Endotracheal Intubation: Sequence allow visualisation of the glottis and enable intuba-
of Events tion under direct vision. The laryngoscope is held in
The salient sequence of events during an uncompli- the left hand and the blade is inserted into the oral
cated tracheal intubation on the intensive care unit is cavity to the right side of the midline, which allows
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Table 8.4 Cormack and Lehane classification of The endotracheal tube should be sited to roughly
laryngoscopy view 2 cm above the carina. Once capnography has con-
Grade 1 Full view of vocal cords/glottis firmed placement within the patient’s airway, clinical
Grade 2 Only posterior commissure/arytenoid cartilages examination can be used to avoid endobronchial intu-
visible bation, but in difficult cases or where there is doubt,
Grade 3 Only epiglottis visible fibreoptic bronchoscopy can be used to ensure opti-
Grade 4 No glottic structure visible mal placement above the carina. Too far in and flex-
ion of the patient’s neck may cause contact with the
carina causing irritation and bronchospasm or right
distraction of the tongue to the left. The tip is then main bronchial intubation. If the tube is not advanced
slowly advanced over the base of the tongue and into far enough into the trachea, extension of the neck can
the valecula, where an anterior vector force is applied lead to inadvertent extubation.
to remove the tongue from the line of sight. The
laryngeal view is graded according to the Cormack
and Lehane classification (Table 8.4). Poor views can
Difficult Intubation
often be improved by external laryngeal manipulation A difficult intubation is defined as an inability to
(BURP; backwards, upwards and rightward pressure secure the airway with an endotracheal tube follow-
on the thyroid cartilage) or a reduction in cricoid ing three attempts, and occurs more commonly in
pressure. With grade 3 and 4 views, the glottic aper- critically ill patients. Repeated intubation attempts
ture is not visualised and advanced airway equipment (more than three) can lead to airway oedema or bleed-
such as videolaryngoscopes and fibreoptic scopes may ing, which will worsen visualisation with subsequent
be required to aid intubation. attempts. Expert help needs to be sought early, and
the priority is to oxygenate via bag-mask ventilation
Confirming Correct Positioning aided by airway manoeuvres (jaw thrust, head tilt–
chin lift) and adjuncts (oropharyngeal, nasopharyn-
It is crucial to confirm that the endotracheal tube is in
geal airways), or ventilation via a supraglottic device.
the trachea as opposed to the oesophagus following
Management should follow local and national proto-
intubation. The most reliable test confirming correct
cols (see Further Reading).
positioning is six successive carbon dioxide traces on
If ventilation and oxygenation are satisfactory, a
the capnograph with a value for end-tidal carbon diox-
definitive airway is required by another technique.
ide (EtCO2) that corresponds to that expected for the
Allowing the patient to wake up (recommended in the
patient. The absence of CO2 on the capnograph trace
elective setting) is unlikely to be an appropriate option
should prompt immediate suspicion of incorrect tube
in the critically ill patient.
position, with direct laryngoscopy or fibreoptic bron-
Advanced airway options available to secure a
choscopy to resite the tube into the trachea. Failure to
definitive airway in the ‘can’t intubate, can ventilate’
recognise oesophageal intubation will result in severe
scenario include the following.
hypoxia within minutes followed by cardiac arrest and
death. Clinical signs such as chest wall movement and 1. Videolaryngoscopy There are a number of
breath sounds on auscultation, and misting within the videolaryngoscopes available to aid intubation. All
tube, as well as appropriate compliance of the inflat- contain a distal light source and camera to allow
ing bag are of value, but can all occur and give false indirect visualisation of the glottis on a screen.
reassurance with oesophageal intubation. Extra care is These devices obviate the need for a direct line of
needed to confirm correct tube placement in patients sight in order to intubate.
in cardiac arrest undergoing CPR, or patients who are 2. Asleep fibreoptic intubation A fibrescope preloaded
on venoarterial extracorporeal membrane oxygena- with an endotracheal tube can be passed either
tion (VA ECMO) support since the value for EtCO2 orally or nasally under direct vision into the
on the capnograph trace will be lower than normal trachea.
despite a correctly sited endotracheal tube (reduced 3. Intubation through the existing laryngeal
pulmonary blood flow). If the value for EtCO2 is <2 mask airway An Aintree catheter (hollow bougie)
kPa, extra steps should be taken to ensure that tube can be loaded on to a fibrescope and the whole
placement is correct. unit passed through the lumen of the ventilating
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63
laryngeal mask airway and into the trachea under scalpel incision through the cricothyroid
direct vision. Upon removal of the fibrescope, an membrane. Caudal traction on the membrane
endotracheal tube can then be passed over the can then be applied from a tracheal hook to allow
Aintree catheter. intubation with a size 6 mm ID cuffed tracheal or
4. Intubating laryngeal mask airway The intubating tracheostomy tube.
laryngeal mask airway is specifically designed to
allow an endotracheal tube to blindly pass through Managing the Intubated Patient
its lumen into the trachea.
Attention to the endotracheal tube needs to be main-
5. Tracheostomy Tracheostomies are usually tained following intubation in order to prevent airway
performed electively on intubated patients. related morbidity. Continuous waveform capnog-
However in the difficult intubation scenario in raphy should be used for every intubated patient to
the critically ill, there may be a case for direct ensure correct tube positioning and allow surveil-
tracheostomy formation whilst ventilating with a lance against tube migration. Endobronchial intuba-
laryngeal mask airway. tion should be monitored for using auscultation, and
chest X-ray. Checking the cuff pressure regularly is
Failed Ventilation important since excessive pressures can cause tracheal
Failure of ventilation is defined as the inability to mucosal damage, whereas an inadequate pressure
maintain oxygen saturations above 90% (if initially can lead to microaspirates and ineffective ventila-
above this value) whilst administering 100% oxygen tion. Cuff pressures between 20 and 30 cmH2O are
using a facemask or laryngeal mask airway. recommended.
Failed ventilation with increasing hypoxaemia in To reduce the risk of inadvertent extubation, judi-
the setting of a difficult intubation, the ‘can’t intubate, cious use of sedation is required as well as care when
can’t oxygenate’ scenario, is a rare but life threatening moving patients.
emergency. The immediate priority is to achieve oxy-
genation and since the upper airway route has failed,
an invasive approach via the cricothyroid membrane Extubation
is recommended. The cricothyroid membrane lies Tracheal extubation is the process of removing the
inferior to the vocal cords, is relatively avascular and endotracheal tube to allow the patient to protect and
can normally be easily located below the thyroid carti- maintain their own airway. To increase the likelihood
lage and above the cricoid cartilage. of a successful extubation on the intensive care unit, a
There are three types of cricothyroidotomy number of criteria firstly need to be met:
approach: 1. Indication for intubation has been corrected,
1. Small cannula devices (2–3 mm ID) Kink resistant 2. Haemodynamic stability,
cannulae can be directed caudally into the trachea 3. Adequate ability to cough and clear secretions,
and their position confirmed by aspirating air 4. Neurologically appropriate,
freely. The resistance through these narrow 5. Adequate oxygenation without requiring high
devices is large, so a high pressure (2–4 bar) levels of PEEP/FiO2,
oxygen source is needed to oxygenate. Some 6. Fully rewarmed (i.e. after cardiac surgery),
degree of upper airway patency is required to 7. Minimal chest drain output.
allow passive exhalation. This limits their use A spontaneous breathing trial can then be performed
beyond short-term rescue oxygenation. using a T-piece or low-level pressure support and
2. Large-bore devices (>4 mm ID) These devices are low PEEP to determine the likelihood of extubation
inserted using either the Seldinger or cannula- success.
over-needle technique. The larger diameter A backup reintubation plan should always be part
accommodates a 15 mm standard breathing of the extubation strategy as it may be more difficult
circuit, which allows the patient to be effectively than the original intubation. Tracheal extubation in
low pressure ventilated. the presence of a known difficult airway can be per-
3. Surgical cricothyroidotomy (>6 mm ID) The formed over an airway exchange catheter, which may
surgical approach involves making a horizontal be tolerated for up to 72 hours.
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To perform an extubation in an uncomplicated Other indications for tracheostomy include failure

airway, the patient should be given 100% oxygen for of protective airway reflexes, management of excessive
at least 3 minutes and the nasogastric tube (if pre- secretions and relief of upper airway obstruction.
sent) should be suctioned. Gentle positive pressure
should be applied followed by cuff deflation and con-
trolled tube removal. Patients may initially be extu-
Tracheostomy Tubes
bated onto a facemask and Waters circuit with 100% Tracheostomy tubes are made from either polyvinyl
oxygen in order to assess adequacy of spontaneous chloride, silicone or metal, and are available in a vari-
ventilation. ety of shapes and sizes. When sizing tracheostomy
tubes, important dimensions to consider include the
diameter (inner and outer), length (proximal and dis-
Tracheostomy tal) and curvature.
Tracheostomy refers to the creation of a stoma at The optimal tracheostomy tube size provides
the skin surface, which is in continuity with the tra- the maximum internal diameter to facilitate airflow,
chea. This procedure is commonly performed on the whilst confining the outer diameter to roughly three
cardiothoracic intensive care unit and involves the quarters of the tracheal lumen. This minimises resist-
insertion of a tracheostomy tube usually between the ance across the tube and also allows adequate air-
second and third tracheal rings. Despite being one of flow around the tube during weaning and attempted
the oldest airway interventions, controversy still exists phonation.
regarding the optimal timing, insertion technique and Since the trachea is essentially straight, the tip
type of tracheostomy tube to use. of an inappropriately long and curved tracheostomy
tube can traumatise the anterior tracheal wall, whilst
Advantages shorter tubes can abut posteriorly. To avoid these
Tracheostomy tubes offer a number of practical and problems, angled tracheostomy tubes have a straight
clinical advantages over oral endotracheal tubes when portion designed to lie more anatomically within the
managing the critically ill. trachea.
Tracheostomy tube length is also an important
1. The work of breathing is reduced since the
consideration since patients with large necks often
dead-space and airflow resistance is less than for
need a longer proximal portion, whereas patients with
equivalent sized endotracheal tubes.
tracheal pathology (tracheomalacia) may need extra
2. Suctioning the tracheobronchial tree in patients
distal length to bypass disease.
with a high secretion burden is easier.
Two different sizing systems exist, which can
3. Tracheostomy tubes are well tolerated, which often
cause confusion since one is based on the length (and
allows the sedation and associated adverse effects
taper) of the outer tube, whilst the other refers to the
to be reduced.
internal diameter. As a reference for the clinician and
4. Mouth hygiene is easier to maintain and to avoid sizing errors, the diameters and distinguish-
phonation as well as swallowing is possible. ing features of tracheostomy tubes are marked on the
5. Complications associated with prolonged flange.
translaryngeal intubation such as vocal cord
damage and laryngeal ulceration are avoided. Cuffed and Uncuffed Tubes
In the intensive care setting, most patients will initially
Indications require a cuffed tracheostomy tube to facilitate positive
The most common indication for tracheostomy in pressure ventilation and protect against aspiration. To
the intensive care setting is to facilitate prolonged reduce the risk of tracheal mucosal ischaemia and
mechanical ventilation and weaning. Recent esti- subsequent stenosis, a high volume/low pressure cuff
mates suggest that approximately 5% of patients inflated to a pressure of no more than 20–25 cmH2O
following cardiac surgery require mechanical ven- is recommended. Uncuffed tracheostomy tubes allow
tilation for at least 7 days due to perioperative com- for airway clearance but do not protect from aspira-
plications, often on a background of underlying tion, so are usually reserved for patients with adequate
respiratory disease. bulbar function who are unable to clear secretions.
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65
Single and Double Cannula Tubes Percutaneous Tracheostomy

Tracheostomy tubes can be standalone single Patients are in the supine position and often have a
lumen devices or contain an accompanying inner bolster placed between their shoulders to allow ade-
cannula (double cannula tubes). Double cannula quate neck extension and exposure. Preprocedural
tubes are inherently safer since in the event of ultrasound scanning of the neck is now increasingly
obstruction the inner cannula can be removed com- being used to assess the anterior neck landmarks.
pletely and independently from the outer lumen Sedation needs to be increased to anaesthetic levels
to manage the blockage. For this reason, and to and paralysis should be given. It is important to venti-
facilitate cleaning, it is often the preferred choice late with 100% oxygen.
of tube for patients discharged to a stepdown unit Capnography to confirm correct tube position-
or ward. Many intensive care units now use double ing is mandatory and bronchoscopy through the
cannulas from the outset. It is however important tracheal tube to guide tracheostomy placement is
to appreciate that the addition of an inner cannula recommended. In order to accommodate the tra-
reduces the functional internal diameter of the tracheostomy tube, the endotracheal tube needs to be
cheostomy tube, which increases airflow resistance withdrawn under bronchoscopic guidance so the tip
and the work of breathing. Furthermore, in some lies at the level of the cricoid cartilage prior to nee-
designs, attachment to the ventilator is only possi- dle puncture.
ble when the inner tube and its associated 15 mm All percutaneous tracheostomy tube placements
connector is in place. are based on the Seldinger technique, with initial
needle aspiration and guidewire insertion midway
Fenestrated and Non-fenestrated Tubes between the cricoid cartilage and sternal notch. This
Fenestrated tracheostomy tubes have single or multi- usually correlates to the space between the second and
ple openings located posteriorly and above the cuff. third tracheal rings. Tract dilatation and tracheos-
Following cuff deflation during spontaneous ven- tomy railroading can be performed using single step
tilation, the fenestrations encourage maximal air- or sequential dilators, balloon inflation, forceps dila-
flow through the larynx to allow phonation and an tation, or by the retrograde translaryngeal approach.
assessment of native airway patency in preparation
for decannulation. Fenestrated tracheostomy tubes Surgical Tracheostomy
are often used in conjunction with one-way speak- This procedure is often performed in an operating
ing valves. These valves cap the tracheostomy tube room under general anaesthesia. A vertical inci-
and allow inspiration but close on expiration, which sion below the cricoid cartilage is usually made and
directs airflow through the larynx when the patient following blunt dissection down, the strap muscles
exhales. Non-fenestrated inner tubes should be used and thyroid isthmus are retracted to expose the tra-
if positive pressure ventilation is required to avoid chea for tracheostomy placement. Open-ended stay
air leaks. sutures can be sited either side of the tracheal stoma
to facilitate postoperative tube reinsertion in case of
Insertion Technique displacement.
Tracheostomies can be performed as open surgical
procedures, most commonly in the operating theatre Timing
or percutaneously at the bedside. Controversy exists as to when the optimal time is to
Both procedures carry low complication rates in perform tracheostomy placement. The benefit of a
experienced hands and individual unit practice is tracheostomy over prolonged translaryngeal intuba-
largely determined by resource and local preference. tion needs to be balanced against the likelihood of
The percutaneous approach is logistically easier the patient needing extended ventilation and the risks
and proponents suggest that peristomal bleeding associated with the procedure.
and infection rates are lower. Surgical tracheosto- The largest randomised controlled trial to date
mies, however, are more appropriate in patients (Tracman) found no benefit in performing early
with difficult neck anatomy and in the emergency tracheostomies within 4 days, and suggested delay-
scenario. ing this procedure until day 10 of translaryngeal
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ventilation. The initial tracheostomy tube is usually Prior to allowing oral feeding, patients need to be able
cuffed, non-fenestrated and may be either single or to tolerate cuff deflation and should have passed a
double cannula in design. It is recommended that bedside swallowing assessment by a speech therapist.
the first routine tube change should not be per-
formed within 4 days after a surgical tracheostomy Weaning and Decannulation
and 7–10 days after a percutaneous one to allow the There is no clear consensus on the optimal trache-
stoma and tract to be established first. The decision to ostomy weaning protocol and different units vary in
change the tracheostomy tube should be multidisci- their practice. The overriding theme is to gradually
plinary, based on the weaning, swallowing and venti- reduce ventilatory support and encourage normal air-
latory needs of the patient. For the first tube change flow patterns in the upper airways to such an extent
or if there are anticipated difficulties, the exchange is that the patient can manage without the tracheostomy
usually performed over a guide such as a gum-elastic tube. This involves increasing periods of cuff defla-
bougie, exchange catheter or suction tubing. With tion, changing to smaller diameter and fenestrated
well-established tracts a guide is not usually needed. tubes, and using speaking valves or caps. A success-
During all tube exchanges, however, there needs to be ful wean requires patient commitment and regular
the necessary equipment and personnel available to multidisciplinary input from nurses, physiotherapists,
manage failure. speech therapist, intensivists and surgeons.
Decannulation should occur as soon as the trache-
Tracheostomy Management ostomy tube is no longer required and it is safe to do
A large proportion of adverse airway events on the so. This occurs at the end of a successful wean, with
intensive care unit involve tracheostomies and can be multidisciplinary team agreement and when core
fatal. To minimise the risk of accidental decannulation criteria have been met (Table 8.5). It is advisable to
or migration, the tracheostomy tube should be safely decannulate during the morning when the patient is
secured with sutures or an approved tracheostomy fasted and can be observed during the day with equip-
tube holder. Sedation should be used judiciously and ment and expertise to manage any complications to
care taken upon patient rolling and moving. In case hand.
of accidental tracheostomy dislodgement or removal,
the safest approach is oral reintubation of the trachea Summary
to stabilise the situation. The establishment and maintenance of a patent airway
Humidified air should be given in order to prevent with ventilation to the lungs is a critically important
the formation of excessively viscous secretions, which first step in the management of a patient on the car-
can obstruct the tube. Heat and moisture exchangers diothoracic intensive care unit. Capnography is an
can be used for this purpose in patients who are either essential adjunct for any patient receiving artificial
self-ventilating or needing ventilator support. To help
manage especially thick secretions, heated water baths
may be needed. Intermittent suctioning and physi- Table 8.5 Patient decannulation criteria
otherapy at intervals dependent on patient secretion
Able to maintain and protect their own airway
burden is also beneficial. The management of sus-
Adequate respiratory function, free from ventilator support
pected dislodgement should follow guidance from the
National Tracheostomy Safety Project (Figure 8.1 and Haemodynamically stable
Chapter 26 Airway Emergencies). Absence of fever or active infection
Consistently alert
Swallowing Strong cough
Swallowing allows early establishment of oral feed- Competent swallow

ing and contributes to the psychological well being Clinically stable
of patients with tracheostomy tubes. However, these No forthcoming procedures requiring anaesthesia (within
patients are at risk of aspiration since the tube and 7–10 days)
cuff can impede normal laryngeal movements during Adapted from the National Tracheostomy Patient Safety
swallowing as well as cause oesophageal compression. Manual 2013.
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67
Emergency tracheostomy management – Patent upper airway
Call for airway expert help

Look, listen & feel at the mouth and tracheostomy
A Mapleson C system (e.g. ‘Waters circuit’) may help assessment if available
Use waveform capnography when available: exhaled carbon dioxide indicates a patent or partially patent airway
No Is the patient breathing? Yes
Call Resuscitation Team Apply high flow oxygen to BOTH

CPR if no pulse/signs of life the face and the tracheostomy
Assess tracheostomy patency
Remove speaking valve or cap (if present)

Remove inner tube
Some inner tubes need re-inserting to connect to breathing circuits
The tracheostomy tube is patent

Can you pass a suction catheter? Yes Perform tracheal suction
Consider partial obstruction
No Ventilate (via tracheostomy) if
not breathing
Deflate the cuff (if present) Continue ABCDE assessment
Use waveform capnography or Mapleson C if available
Tracheostomy tube partially

Yes obstructed or displaced
Is the patient stable or improving? Continue ABCDE assessment
No
REMOVE THE TRACHEOSTOMY TUBE
Look, listen & feel at the mouth and tracheostomy. Ensure oxygen re-applied to face and stoma
Call Resuscitation team No Yes Continue ABCDE

Is the patient breathing?
CPR if no pulse/signs of life assessment
Primary emergency oxygenation Secondary emergency oxygenation
Standard ORAL airway manoeuvres Attempt ORAL intubation

Cover the stoma (swabs/hand). Use: Prepare for difficult intubation
Bag-valve-mask Uncut tube, advanced beyond stoma
Oral or nasal airway adjuncts
Supraglottic airway device e.g. LMA
Attempt intubation of STOMA

Small tracheostomy tube/6.0 cuffed ETT
Tracheostomy STOMA ventilation
Consider Aintree catheter and fibreoptic
Paediatric face mask applied to stoma ‘scope/Bougie/Airway exchange catheter
LMA applied to stoma
National Tracheostomy Safety Project. Review date 1/4/14. Feedback & resources at www. tracheostomy.org.uk
Figure 8.1 Emergency tracheostomy management. Reproduced from McGrath et al. Anaesthesia. 2012; 67: 1025–1041, with permission
from the Association of Anaesthetists of Great Britain & Ireland/Blackwell Publishing Ltd. (A black and white version of this figure will appear
in some formats. For the colour version, please refer to the plate section.)
13:49:14
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68
ventilatory support via an endotracheal tube or tra-

cheostomy tube. Extra care must be taken not to miss
Further Reading
tube dislodgement in the setting of reduced CO2 deliv- American Society of Anesthesiologists Task Force on
Management of the Difficult Airway. Practice
ery to the lungs, i.e. in cardiac arrest, or in VA-ECMO
Guidelines for Management of the Difficult
support. Anticoagulation can increase the risk of Airway: An Updated Report. Anesthesiology. 2013;
bleeding into the airway following manipulation, and 118: 1–20.
extra care is required in these patients. Cook TM, Woodall N, Frerk C; 4th National Audit Project
of The Royal College of Anaesthetists and the Difficult
Learning Points Airway Society. Major complications of airway
• Equipment for emergency intubation should management in the United Kingdom. Report and
findings March 2011. Available from: www.rcoa.ac.uk/
be immediately available in the cardiothoracic document-store/nap4-full-report
critical care unit alongside equipment for
Difficult Airway Society UK Guidelines. 2015. Available
management of the difficult airway.
from: www.das.uk.com/guidelines/downloads.html
• Extra care is needed to avoid airway bleeding in
McGrath BA, Bates L, Atkinson D, et al. Multidisciplinary
patients receiving anticoagulation.
guidelines for the management of tracheostomy and
• Oesophageal intubation may be difficult to laryngectomy airway emergencies. Anaesthesia. 2012;
diagnose in the presence of low pulmonary blood 67: 1025–1041.
flow: use direct assessment via laryngoscopy or Young D, Harrison DA, Cuthbertson BH, et al. Effect
fibreoptic bronchoscopy in case of doubt. of early vs late tracheostomy placement on survival
• Management of the difficult airway should follow in patients receiving mechanical ventilation. The
local and national guidance. Tracman randomized trial. Journal of the American
• Safe airway management requires Medical Association. 2013; 309: 2121–2129.
multidisciplinary input.
MCQs
Please identify whether the below statements are true or (c) Decannulation can occur as soon as the patient is
false. weaned from positive pressure ventilation
1. Difficult intubation management in the cardiotho- (d) The tube with deflated cuff should be a tight fit in
racic critical care unit should involve: the trachea so that no air can escape around it
(a) At least five attempts at intubation before help 3. Endotracheal intubation:

is called (a) Requires specific training under supervision by an
(b) A logical approach guided by local and national expert in airway management
protocols (b) Should always be performed by an anaesthetist
(c) Preparation of the patient, equipment, drugs and (c) Should always have waveform capnography avail-
team if time allows able continuously to aid with assessment of tube
(d) Administration of the same doses of induction position
agents as in an elective setting (d) Requires chest X-ray to exclude oesophageal
(e) Clear communication of team roles intubation
2. Regarding tracheostomy: (e) Can be more difficult to perform in the critically ill
patient
(a) A fenestrated inner tube should be used with posi-
tive pressure ventilation 4. Cardiothoracic patients may experience airway com-
plications due to:
(b) Tracheostomy should be performed routinely after
4 days of endotracheal intubation (a) Presence of anticoagulation
13:49:14
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69
(b) Low pulmonary blood flow reducing the level of 5. Predictors of difficult intubation include:
expected end-tidal carbon dioxide (a) Limited neck extension
(c) Airway oedema secondary to critical illness (b) Prominent overbite
(d) Cerebrovascular accident following surgery (c) Short legs
(e) Prolonged endotracheal intubation (d) Marfan’s syndrome
(e) Mallampati score of I
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Chest Drainage
Chapter
9 Alia Noorani and Yasir Abu-Omar
Introduction Table 9.1 Common indications for chest drainage
The pleural space is a thin, fluid filled space between Traumatic haemothorax
the visceral and parietal pleura. In a healthy 70 kg Large spontaneous or traumatic pneumothorax
individual, this space contains a few millilitres of Benign or malignant pleural effusion
serous pleural fluid, the function of which is to allow Chylothorax
the pleurae to slide easily over the lungs during ven- Following cardiac or thoracic surgery
tilation. The presence of air or fluid (pus, blood, chyle
or excessive pleural fluid) impedes the normal func-
tion of the lungs, and depending on the symptoms and Figure 9.1a shows a chest radiograph of a patient
signs affecting the patient, will require chest drainage. with a large pneumothorax following cardiac surgery,
Usually, the pressure in the pleural space is less and Figure 9.1b shows the same patient post chest
than atmospheric. This negative pressure helps main- drain insertion. Figure 9.2a shows a chest radiograph
tain partial lung expansion and the magnitude of of a patient with a left pleural effusion and Figure 9.2b
negativity changes during the respiratory cycle. In shows the same patient post drain insertion.
inspiration the pressure is approximately −8 cmH2O
and in expiration this falls to −4 cmH20. A breach of Technique
the pleural cavity leads to development of a positive The emergency insertion of a large bore chest drain for
pressure in this space either equal to or more than the relief of a tension pneumothorax is well described
atmospheric pressure, leading to a pneumothorax. in the Advanced Trauma Life Support guidelines and
there are many published step-by-step descriptions of
History the procedure.
The earliest known reference to chest drainage dates The British Thoracic Society guidelines for the
back to the fifth century Hippocratic texts. Here con- insertion of chest drains were originally developed in
servative management of empyemas is described 2003 and subsequently updated in 2010. These guide-
using plants and herbs, and open drainage for per- lines were in effect aimed at training and guiding phy-
sistent infections is well documented including the sicians to safely perform this procedure. Figure 9.3
surgical technique for doing this. Hippocrates gave shows the BTS guidelines as an algorithm.
detailed descriptions of using a scalpel to cut between
the ribs, evacuating pus and leaving a hollow tube in Anatomical Landmarks
for 2 weeks. The BTS describes the triangle of safety within which
Since this, other physicians have described the chest drains should be placed (Figure 9.4). This trian-
technique including the leading French physician sur- gle is the area bounded by the anterior border of latis-
geon Guy de Chauliac in 1395. The first description of simus dorsi and the lateral edge of pectoralis major
a closed chest drainage system was by Hewett in 1876. with the base formed by a line superior to the horizon-
tal line of the nipple.
Indications The advantages of this position are to minimise
The indications for chest drain insertion are to remove potential damage to underlying nerve and vascular
fluid, air or both from the pleural space. Table 9.1 structures such as the long thoracic nerve and the lat-
shows the common indications for chest drainage. eral thoracic artery. Additionally, placement in this
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Chapter 9: Chest Drainage
Figure 9.1 (a) Radiograph of a patient with a large right pneumothorax (black arrows). (b) The same patient with a right sided chest drain in
situ (white arrow) and reinflation of the right lung.
Figure 9.2 (a) Chest radiograph of a patient with a large right pleural effusion (black arrows) and (b) resolution of the effusion with the
insertion of a right sided chest drain (black arrows).
area may prevent excessive breast or muscle tissue premedication prior to the procedure can include
dissection, reducing the risk of scarring. The pres- midazolam or an opioid. Caution with these drugs
ence of a loculated effusion may require a more pos- should be exercised in patients with underlying res-
terior drain placement but this should be undertaken piratory disease.
under the supervision of a specialist or under image Patients with abnormal coagulation or platelet
guidance. Posteriorly placed drains are more likely to defects should have these corrected before an elective
cause discomfort. drain insertion, and for those on warfarin the INR
should be allowed to reach 1.5 or below if possible.
Preinsertion Preparation
All patients requiring a chest drain should be con- Patient Positioning
sented for the procedure (unless unable to do so The ideal position for drain insertion is with the
due to their clinical status) and this consent should patient upright or at a 45° angle, with the arm on the
be recorded in the clinical notes. Appropriate affected side abducted and externally rotated and
13:50:40 71
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Insertion of Chest Drain
Pneumothorax or pleural fluid requiring drainage
Does this need to be done YES

as an emergency? Insert drain
(e.g. tension)
NO
Consider pleural aspiration to relieve

YES Does the patient have YES symptoms and delay a drain insertion
Is it outside of normal
significant respiratory until working hours and when appropriate
working hours?
compromise? expertise and/or supervision is available
NO NO
Requirements for Insertion
Delay procedure
Prepare patient for chest drainage of Chest Drain
until working hours
Written consent
Clean area to perform procedure
Is the drain required for Insert drain Competent operator or supervisor
fluid? NO Nursing staff familiar with drain management
YES
Equipment Required for Chest Drain
Insertion
Is the operator Seek senior
experienced? help 1% lidocaine
NO
Alcohol based skin cleanser x2 coats
YES Sterile drapes, gown, gloves
Needles, syringes, gauze swabs
Scalpel, suture (0 or 1–0 silk)
Insert drain.
Chest tube kit
Ultrasound guidance
Closed system drain (including water) and tubing
strongly recommended.
Dressing
Clamp
Figure 9.3 British Thoracic Society algorithm for the insertion of chest drains.
placed behind the patient’s head. This exposes the

axillary area.
Prior to insertion it is imperative to undertake a
clinical examination to confirm the presence of pleu-
ral fluid or pneumothorax and to confirm the side of
the pathology on a recent chest radiograph. The only
exception is in the case of a tension pneumothorax
where clinical signs alone are sufficient.
The increasing use of thoracic ultrasonogra-
phy to identify the presence of an effusion is highly
recommended.
Procedure
1. Once the patient is positioned appropriately, the
triangle of safety is prepped with antiseptic and
draped. The entire procedure must be carried out
Figure 9.4 The triangle of safety. Anteriorly the lateral border of
pectoralis major, laterally the anterior border of latissimus dorsi and in an aseptic manner to avoid infection ascending
inferiorly a line superior to the fourth nipple. into the thoracic cavity. The rates of empyema
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following chest drain insertion after trauma skin incision just above and parallel to the ribs is
are approximately 3% and lead to significant made. This incision should be similar in size to the
morbidity. One study has identified no infections diameter of tube being inserted and the operator’s
in a group of 80 patients requiring a chest drain index finger.
for trauma carried out in an aseptic manner. 5. Much debate has been had about the size of the
2. The procedure equipment is usually available chest tubes used. General recommendations are
sterile and prepacked in most hospitals. Chest to use a large bore tube in the setting of trauma
tubes are made of clear plastic and are available in or acute haemothorax, to facilitate drainage
a variety of sizes (diameters) based on the French and monitor on-going losses (28–30F). Smaller
scale (multiples of 4, e.g. 12F, 16F, 20F, up to 36F). drains are more comfortable and can be used for
These drains have multiple side holes to allow pneumothoraces. Blunt dissection into the pleural
effective drainage and have a radio-opaque marker cavity, skirting the upper border of the ribs to
strip to help identification on chest radiography. avoid injury to the neurovascular bundle, should
Trocars are occasionally present within chest be performed, with a finger sweep manoeuvre into
drains but the routine use of these is not the pleural space, in particular with larger drains,
recommended as they can cause undue visceral to avoid injury to the lung parenchyma and other
damage. thoracic organs.
6. Once a chest drain is inserted into the
The kit should contain:
pleural cavity it should be connected to an
• Sterile drapes underwater seal and secured to the skin. A chest
• 1% lidocaine (in a dose of up to 2 mg/kg) radiograph should be requested to assess the
• 20 ml syringe position.
• Green and yellow needles (21–25 gauge)
• Sterile skin preparation solution Underwater Seals
(chlorhexidene) All chest drains should be connected to a single flow
• Scalpel drainage system which can comprise an underwater
• Curved instrument such as a Roberts’s clamp seal bottle or a flutter valve. The purpose of such a
or Spencer Wells system is to maintain a negative intrapleural pressure
• Chest drain (sizes vary, usually 28F and larger and although there are different methods of achiev-
for effusions and smaller for pneumothorax) ing this, in a traditional underwater seal, a tube is
• Skin suture (nylon or silk) placed at a depth of 3 cm with a side vent that allows
• Chest drain tubing the escape of air. Often a suction system is required
• Chest drain bottle primed with sterile water to maintain a negative pressure. The newer thoracic
(underwater seal) drainage systems such as the Thopaz (Medela, IL) are
• Dressing to cover drain insertion site. compact devices that allow for patient mobility, with-
out restriction.
3. Next, local anaesthesia is infiltrated using a
small gauge needle and by raising a dermal bleb.
Lidocaine in a safe dose (up to 2 mg/kg) or an Contraindications
alternative local anaesthetic is used. The next There are no contraindications to chest drain inser-
step is to freely aspirate either air in the case of tion in a clinically urgent scenario. For non-urgent
pneumothorax or fluid in the case of an effusion cases, however, if a patient is anticoagulated, the INR
to confirm the pathology. If neither can be done, a should be less than 1.5. Any other clotting abnormali-
chest drain should not be inserted without further ties should also be corrected.
image guidance. Studies have shown that image
guided placement of drains has a low complication Nursing Care
rate of pneumothorax at 3% and a successful The aftercare of chest drains is extremely important.
insertion rate of over 70%. Patients should be managed on a ward where staff
4. Once a successful aspirate has been obtained are experienced in the routine care of chest drains.
and the local anaesthetic deemed successful, a A daily record of the volume of drainage, the type
13:50:40 73
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of fluid drained and the presence or absence of an

air leak and swing should be clearly documented to
Drain Malposition
Malpositioning of drains is the commonest complica-
facilitate decision making with regards to the timing
tion of chest drain insertion and understandably this
of drain removal. Additionally, drains should rou-
is commoner in the emergency setting than the elec-
tinely be inspected for non-function as heralded by
tive setting where the speed of the procedure can lead
lack of fluctuation of fluid within the tube with res-
to injury. Intraparenchymal positioning of drains can
piration or coughing. Non-function may be due to
occur in the presence of pleural adhesions. Chest wall
kinking, debris or malposition. Tension pneumotho-
placement has been reported to occur in up to 18%
rax is a serious complication within the context of an
of cases and can be diagnosed with a lack of swinging
on-going air leak and a blocked drain. Due care with
in the drain tubing and bottle. Drains placed too far
adequate fixation of the drain and subsequent patient
into the chest cavity can result in perforation of other
education are important to avoid inadvertent chest
intrathoracic organs such as the heart, major vessels,
drain dislodgement.
nerves, and oesophagus as well as the diaphragm.
Abdominal placement of drains can occur when the
Removal of Drains insertion point is lower than the base of the triangle of
Chest drains should be removed once the clinical indi- safety. Injury to the liver, spleen, stomach and bowel
cation for their use has been fulfilled. For pneumotho- have all been reported.
races this is when the lung has reinflated on the chest
radiograph and when the drain has stopped bubbling.
For pleural effusions this depends on the pathology
Nerve Injuries
that prompted drain insertion and the volume of Horner’s syndrome has been reported due to direct
fluid drained. An empyema will require a prolonged pressure of the tip of the chest tube on the sympathetic
period of drainage compared to a postoperative drain chain in the medial portion of the apex of the thoracic
inserted in a cardiac patient. cavity. Phrenic nerve injury can cause diaphragmatic
Chest drain removal is a two-person job whereby paralysis and severe cases may require plication.
both professionals are trained in the procedure. Injury to the long thoracic nerve of Bell during inser-
One removes the drain while the patient performs tion too far laterally in the triangle of safety can lead
a Valsalva or during expiration. The assistant then to winging of the scapula. Ulnar neuropathy due to
pulls the purse string present and ties it to close the injury of the posterior cord of the brachial plexus has
insertion site. also been reported.
Complications Heart
Chest drainage is a fairly common procedure but Inadvertent injury to the heart is a potentially fatal
it is not without risk. The NPSA reported over 2000 complication of chest drain insertion. Injuries to all
patient safety incidents relating to chest drains chambers have been reported and the continued
between January 2005 and March 2008. Of these there drainage of fresh blood should raise the suspicion of
were 12 deaths and 15 cases of severe harm associated this injury. Urgent surgical intervention is required.
with chest drains between January 2005 and March
2008. The main reasons for these incidents were Intercostal Vessels
deemed to be: Injury to the intercostal vessels can lead to significant
• Inadequate level of supervision, training or haemorrhage. Knowledge of intercostal bundle anat-
operator experience, omy and the technique of dissecting above a rib are
• Incorrect site of insertion and poor patient essential to avoid this complication.
positioning,
• Inadequate preprocedure imaging, Re-expansion Pulmonary Oedema
• Excessive insertion of the dilator when using a This is an uncommon but potentially fatal complica-
Seldinger technique. tion following chest drain insertion for pleural effu-
Details of some complications are given below. sion or pneumothorax. Mortality rates of up to 20%
13:50:40
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75
have been reported. The aetiology of re-expansion in up to 8% of cases. Cases of infection are higher for
pulmonary oedema is unclear and it can affect the emergency insertions of drains than for elective proce-
ipsilateral, contralateral or both lungs. It is thought dures. Routine antibiotics are not indicated, except in
that increased endothelial permeability and loss of trauma cases where gross contamination is expected.
alveolar integrity are the main factors leading to
exudation of proteinaceous fluid. Rapid drainage Summary
of large volumes of pleural fluid resulting in sudden Chest drain insertion is a vital part of the management
re-expansion may be a contributing factor as can re- of the trauma, cardiothoracic surgical and chest medical
expansion of a lung which has been collapsed for sev- patient. It should be undertaken by experienced opera-
eral days. Clinical findings can be quite profound with tors to avoid significant injury to other intrathoracic or
the patient developing symptoms and signs within 2 intra-abdominal structures leading to morbidity and
hours following chest drainage and lung re-expansion. mortality. Routine aftercare should be undertaken by
Signs include tachypnoea, tachycardia and central experienced staff who can monitor the functionality of
cyanosis. Chest radiography may show ground glass the drain and observe closely for complications.
appearance. Close cardiorespiratory monitoring with
symptomatic support is key to survival.
Further Reading
Oesophageal Perforation Adegboye VO, Falade A, Osinusi K, Obajimi MO.
Reexpansion pulmonary oedema as a complication
This is a rare complication following chest drain inser- of pleural drainage. Nigerian Postgraduate Medical
tion. The drainage of enteric contents should raise the Journal. 2002; 9: 214–220.
suspicion of an injury and contrast imaging will con- Havelock T, Teoh R, Laws D, Gleeson F. Pleural procedures
firm the diagnosis. and thoracic ultrasound: British Thoracic Society
Pleural Disease Guideline 2010. Thorax. 2010;
Chylothorax 65(Suppl 2): 61–76.
Injury to the thoracic duct can lead to the development of Hewett FC. Thoracentesis: the plan of continuous
aspiration. British Medical Journal. 1876; 1: 317.
chylothorax. Appropriate investigations include medium
chain triglycerides levels, which directly enter the portal Kesieme EB, Dongo A, Ezemba N, et al. Tube
thoracostomy: complications and its management.
system, thereby avoiding the lymphatic system.
Pulmonary Medicine. 2012; 256878.
Lamont T, Surkitt-Parr M, Scarpello J, et al. Insertion of
Infection chest drains: summary of a safety report from the
Ascending infection leading to empyema is a serious National Patient Safety Agency. British Medical Journal.
complication following chest drainage and can occur 2009; 339: b4923.
MCQs
1. Indications for insertion of a chest drain include: (b) Lateral border of serratius anterior, medial border
(a) Pneumothorax of latissimus dorsi and superiorly the nipple
(b) Chylothorax (c) Medial border of pectoralis minor, lateral border of

pectoralis major and the sixth costal interspace
(c) Empyema
(d) None of the above
(d) Haemothorax
3. The commonest complication of chest drain insertion is:
(e) All of the above
(a) Malposition
2. The boundaries of the triangle of safety are:
(b) Bleeding
(a) Anterior border of latissimus dorsi, lateral border
of pectoralis major and inferiorly a line superior to (c) Infection
the nipple (d) Tension pneumothorax
13:50:40 75
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76
4. The purpose of an underwater seal is to: minutes. You are asked to see her because she is in
(a) Maintain a positive intrapleural pressure respiratory distress with tachypnoea, tachycardia and
mild cyanosis. The most likely cause for this is:
(b) To allow drainage of pleural contents
(a) Tension pneumothorax
(c) To prevent infection
(b) Haemothorax
(d) To maintain a negative intrapleural pressure
(c) Re-expansion pulmonary oedema
5. A 65 year old female had a right chest drain inserted
for a large pleural effusion 2 hours ago. She drained (d) Bronchopleural fistula
3 litres of serosanguinous fluid within the first 45 (e) Cardiac herniation
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77
Cardiac Pacing and Defibrillation

Chapter
10 Sérgio Barra and Patrick Heck
Introduction and these parameters will also influence the urgency

and type of treatment required.
Patients admitted to a cardiothoracic critical care unit
In addition, patients in the cardiothoracic CCU
(CCU) are at increased risk for cardiac arrhythmias
may have previously implanted cardiac electronic
and severe conduction disturbances, which represent
devices such as standard pacemakers, cardiac resyn-
an important cause of morbidity and can be poten-
chronisation therapy (CRT) devices and implantable
tially life threatening. Sustained arrhythmias may
cardioverter-defibrillators (ICD). Although implanta-
occur in up to 20% of critically ill patients admitted
tion, follow-up and troubleshooting of these devices
to the CCU. Atrial fibrillation (AF) and ventricular
should be in the domain of a trained cardiologist, it
tachycardia (VT) represent the majority of tachyar-
is imperative that intensive care physicians are famil-
rhythmias, while conduction disturbances with severe
iar with the patients’ underlying cardiac diagnoses,
bradycardia can account for up to 20%.
the reason for the device implant, the basics of the
These events may represent the primary reason
current cardiac electronic device technology and
for admission, but are often the result of a series of
the most frequent issues relevant in the context of a
insults commonly seen in the context of a CCU, such
cardiothoracic CCU.
as hypoxia, myocardial ischaemia, infection, sepsis,
The purpose of this chapter is to discuss the role
adrenergic hyperactivity, QT interval prolongation
of pacing and defibrillation in patients admitted to a
and electrolyte imbalance. Additional causes or trig-
cardiothoracic CCU and the most frequently encoun-
gers include cardiac surgery, mechanical ventilation,
tered issues involving pacemakers and ICDs.
mechanical irritation from central venous catheters,
inotropic and vasopressor agents and drugs known to
prolong the QT interval. Pacing in the Cardiothoracic Critical
The presence of significant structural heart dis-
ease, chronic obstructive pulmonary disease or other
Care Unit
The most common indication for pacing, either tempo-
significant extracardiac comorbidities, systemic
rary or permanent, is bradycardia. Bradyarrhythmias
inflammatory response syndrome, sepsis, high cen-
are relatively common in patients admitted to the
tral venous pressure and low arterial oxygen tension
CCU following cardiac surgery. In most cases, these
are known predictors of a higher arrhythmic risk.
events are temporary and due to sick sinus syndrome,
However, it is often not possible to predict or prevent
slow AF or atrioventricular (AV) block.
the occurrence of severe arrhythmias or conduction
disturbances and therefore a prompt diagnosis and
treatment are required. Causes of Bradycardia
Management includes the correction of a known The most common cause of bradycardia in the cardio-
trigger as well as treatment directed at the arrhyth- thoracic CCU is postoperative heart block. Up to 8%
mia itself (such as antiarrhythmic drugs, pacing, car- of patients undergoing aortic valve replacement were
dioversion or defibrillation). The impact of a certain shown to require permanent pacemaker implantation.
arrhythmia depends on the patient’s underlying car- Local oedema may prolong conduction times, but direct
diac and respiratory function and the characteristics injury to the conduction system during removal of
of the arrhythmia itself (rate, duration, irregularity), penetrating calcium or insertion of deep stiches placed
13:52:42 77
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during valve surgery are the main cause. Postoperative The cost of prolonged occupation of intensive
complete AV block is seen in approximately 4% of care beds and prolonged hospital stay, as well as the
patients undergoing mitral valve replacement and ring increased morbidity, reduced mobilisation, comfort
annuloplasty, although any degree of AV block may be and safety associated with prolonged temporary pac-
seen in nearly 25%. Damage to the AV nodal artery ing should be weighed against the cost and risks of
may play a role in these cases. Proximal left ante- unnecessary pacemaker implantation in patients who
rior descending artery and septal artery disease have would otherwise demonstrate a full recovery.
also been shown to increase risk of postoperative AV
block. Predictors of need for permanent pacemaker Basic Pacemaker Functioning
implantation include older age, female sex, greater
A detailed review of pacemaker function is beyond
preoperative end-systolic diameter and left ventricu-
the scope of this chapter, but certain considerations
lar septum hypertrophy, pre-existing conduction sys-
regarding basic pacemaker types and function are
tem disease, severe annular calcification, prolonged
worth mentioning. In its simplest form a pacing sys-
total perfusion time, re-do operations and history of
tem delivers regular electrical impulses to the heart at
renal dysfunction, hypertension and bicuspid aortic
a programmed rate. The minimum energy required to
valve. Predictive models have been developed for the
be delivered by the pacing system in order to achieve
prediction of perioperative need for permanent pace-
electrical capture is called the pacing threshold. Most
maker implantation.
modern pacing systems are designed to also look
for intrinsic electrical activity first, before pacing, in
When to Pace order to minimise any unnecessary pacing but also to
prevent delivery of a ventricular pacing stimulus on a
Acutely, the decision to pace is based on the haemody-
T wave, which can be dangerous and trigger arrhyth-
namic impact caused by the underlying bradycardia,
mias. To do this the pacing system has to be able to
rather than the specific rhythm disturbance per se.
sense intrinsic electrical activity.
When pacing is required, it may be temporary or per-
manent. Temporary pacing options include surgically
implanted epicardial pacing wires, transvenous pacing Pacing Mode
leads implanted fluoroscopically or using floatation
Whether permanent implanted systems or tempo-
balloons or, in emergency situations, transcutane-
rary external pacing boxes, all pacing systems have
ous pacing via external defibrillator pads. Decisions
different pacing modes that dictate their function.
on permanent pacemaker implantation are based on
The North American and British Group (NBG) pace-
whether the bradycardia is expected to resolve or not.
maker code is a three-to five-letter code designed to
The American College of Cardiology/American
describe pacemaker mode.
Heart Association guidelines recommend perma-
nent pacemaker implantation for patients with post- • Th
e first letter designates the chamber paced: A
operative third- degree or advanced second- degree stands for atrium, V for ventricle, D for both
AV block that is not expected to resolve, although the (dual), O if the pacemaker has been deactivated.
timing for implant is left to the physician’s discretion. • The second letter designates the chamber sensed
Most authors recommend pacemaker implantation (A, V, D, O): O represents asynchronous pacing
5–7 days after the operation if conduction distur- without sensing.
bances persist, especially in patients in whom these • The third letter describes the pacemaker’s
disturbances are unlikely to recover, namely those at response to a sensed signal: I (inhibition) means
advanced age, with pre-existing conduction system the pacemaker discharge is inhibited by a sensed
disease and submitted to valve surgery. Recovery is signal; T (trigger) means the pacemaker discharge
common in patients with sick sinus syndrome, but is actually triggered by a sensed signal; D (dual)
unlikely in the case of complete heart block. Predictors means both inhibition and triggering responses
of long-term pacemaker dependency are complete are available (for example, in a DDD pacemaker,
AV block as the indication, bypass time longer than an atrial sensed signal will inhibit atrial pacing
105–120 minutes, preoperative history of syncope and but trigger ventricular pacing after a prespecified
body mass index ≥28.5 kg/m2. delay).
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Chapter 10: Cardiac Pacing and Defibrillation
Table 10.1 Pacemaker modes of potential applicability to patients in the cardiothoracic critical care unit
MODE Applicability
AOO and VOO • Asynchronous pacing without any sensing
• Useful during surgery or when a patient is exposed to external sources of noise (such as diathermy)
• AOO should only be selected if the underlying condition is sick sinus syndrome, but with normal AV conduction
VVI • Ventricular demand pacing
• This is the most common mode used for patients with severe bradycardia
• Spontaneous ventricular activity is sensed and therefore there is a low risk of R-on-T phenomenon with
subsequent ventricular arrhythmias
• There is also a low risk of pacemaker mediated tachycardia
• The lack of AV synchrony may reduce cardiac output
DDD • Pacing and sensing in both chambers with AV synchrony
• Optimal pacing mode in patients with sick sinus syndrome or AV block
• The response to DDD pacing depends on the underlying rhythm
• There is a small risk of pacemaker mediated tachycardia
DDI • Sensing occurs in both chambers, but a sensed atrial signal does not trigger ventricular pacing
• Tracking of rapid atrial rates (in patients with atrial fibrillation, atrial flutter or atrial tachycardia) will not occur
• Pacemaker mediated tachycardia is not possible in this mode
• Position four refers to the rate-response algorithm Biventricular pacemakers (also referred to as
and is only relevant for permanent systems. Rate- CRT) deserve special mention. These devices are
response means the pacemaker will be able to indicated in patients who may not actually have any
increase its pacing rate in response to increasing bradycardia, but have a LV ejection fraction ≤35%,
physiological needs. This is possible due to the QRS duration ≥120 ms and heart failure symptoms,
incorporation of either activity sensors with especially in the presence of left bundle branch block.
vibration detectors or minute-ventilation CRT can improve cardiac output, haemodynamics,
sensors. heart failure symptoms, functional capacity and qual-
• Position five is used to indicate whether multisite ity of life in appropriately selected patients. It is there-
pacing is present. fore reasonable to expect that a patient on the CCU
who already has a CRT device in situ has advanced
A three-letter code is adequate to describe emer-
heart failure, and maintaining correct device function
gency temporary pacing and most forms of perma-
in these patients is even more critical.
nent pacing in the context of a cardiothoracic CCU.
Table 10.1 gives examples of pacemaker modes, which
the CCU physician should be familiar with. Although Implantable Cardioverter Defibrillators
the VVI mode is potentially applicable to all cases of ICDs are seeing more widespread use within cardi-
bradycardia, it should be kept in mind that the lack ology and are therefore likely to be seen in patients
of AV synchrony may reduce cardiac output by up to on the cardiothoracic CCU. They are implanted in
25%, which is particularly relevant in patients with patients at high risk of life- threatening ventricu-
structural heart disease. A DDD mode, where possi- lar arrhythmias, most commonly due to structural
ble, will ensure appropriate AV synchrony. heart disease such as ischaemic or dilated cardiomyo
pathies. All ICDs have pacemaker functions in addi-
tion to their defibrillator function. Accordingly, they
Pacemaker Type can be single, dual or biventricular systems.
Permanent pacemakers can be single chamber (usu- Figure 10.1a illustrates a simple single chamber
ally right ventricle), dual chamber (right atrium and pacemaker with a solitary lead in the right ventricle.
right ventricle) or biventricular systems. The choice of Figure 10.1b shows a more complex CRT-D device
system is decided based upon underlying cardiac con- with leads in the right atrium, right ventricle and in
ditions and indication for the device, and will be made a branch of the coronary sinus (for left ventricular
by an appropriately trained cardiologist. pacing).
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(a) (b)
Figure 10.1 Single chamber pacemaker (a) and cardiac resynchronisation therapy defibrillator (b). (a) White arrow, right ventricular lead
placed in the interventricular septum. (b) Black arrow, right atrial lead placed in the right atrial appendage; grey arrow, single-coil ICD lead
placed in the right ventricular apex; white arrow, left ventricular lead placed in a branch of the coronary sinus; black arrow, high-energy
device.
Pacing Related Complications Pacemaker–Patient–Environment

Pacing related complications can either be as a con- Interactions and Special
sequence of the implant procedure itself or due
to abnormal or unexpected pacemaker function. Considerations
Although intensive care physicians do not implant or Certain precautions should be taken when perform-
program pacemakers, it is important to be aware of ing specific procedures or manoeuvres in patients
potential environmental factors that may impact on carrying cardiac electronic devices and this list is by
pacemaker function and possible acute complications no means exhaustive:
related with the temporary or permanent pacing sys- • When externally defibrillating a patient with a
tem implantation. pacemaker the external electrodes should not
be placed close to the pacemaker, the minimal
Implant Complications effective energy should be used and the device
With any transvenous system, permanent or tempo- must be checked afterwards.
rary, the following acute implant related complications • Certain situations may cause a temporary rise
may occur: myocardial perforation with pericardial in pacing threshold and thereby impair device
effusion and tamponade, pneumothorax, haemotho- function, including electrolyte disturbance and
rax, lead displacement or acute infection. immediately after CPR.
• Subclavian puncture should be avoided
Other Complications ipsilateral to implanted devices when inserting
Other potential issues involving patients with pace- a central venous line due to the risk of lead
makers include the precautions needed when per- insulation tear.
forming direct current cardioversion or defibrillation, • Pulmonary artery catheters should also be
the applicability and utility of magnet application, the avoided, if possible, in patients with recent
possibility of electromagnetic interference and appar- device implantations due to the risk of lead
ent or real system malfunction with failure to pace, displacement.
failure to capture, failure to sense or increasing pacing • Atrial pacing spikes might be misinterpreted as
threshold. QRS complexes by intra-aortic balloon pumps
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Table 10.2 Troubleshooting issues encountered in patients with pacemakers
Causes Manifestations Troubleshooting

Failure of • Battery depletion Absence of pacing spikes, with • Perform chest X-ray to exclude lead
output • Component failure or without magnet application fracture
• Total lead fracture Asystole or bradycardia, • Pacemaker interrogation will reveal
• Loose connections between depending on the patient’s battery voltage depletion if true
generator and lead underlying rhythm output failure is due to battery
• Oversensing end-of-life or very high or infinite
impedance in the presence of lead
fracture
• Replace lead or generator if needed
• Reduce sensitivity if oversensing is
the cause of pacing inhibition
Failure to • Increase in pacing threshold above Presence of pacing spikes • Reprogram energy output (increase
capture programmed value without subsequent myocardial voltage output or pulse duration)
• Defective pacing leads (partial capture (shown by the absence • Pacemaker interrogation will reveal
fracture or insulation breach; the of an electrogram) high impedance in the presence of
latter may be caused by central Higher than normal amplitude lead fracture or low impedance if
venous catheter placement through of pacing spikes if insulation insulation failure
subclavian route) failure • Perform chest X-ray to exclude lead
• Battery depletion Asystole or bradycardia, displacement
• Lead displacement depending on the patient’s • Replace lead if needed
• Severe hyperglycaemia, underlying rhythm • Correct electrolyte and metabolic
hyperkalaemia, acidosis and alkalosis disturbances
Rapid pacing • Oversensing of the atrial channel Rapid ventricular paced • Adjust sensitivity to prevent
(due to partial lead fracture or rhythm –there is ‘tracking’ of oversensing
electromagnetic interference) the atrial sensed events • Program pacemaker to VVI or DDI
• Underlying atrial tachyarrhythmia mode to prevent tracking of atrial
with tracking of p waves to the tachyarrhythmia
programmed upper rate limit
and interfere with triggering. Using arterial of sensing. When lack of pacing or lack of capture
waveform is an alternative. are detected, all connections should be immediately
• The use of electrocautery can cause interference checked, the ventricular output set to maximum and
with both pacing and ICD systems. In the generator programmed into asynchronous mode.
pacemakers it might result in inappropriate Lack of capture is usually the result of lead displace-
inhibition of pacing as the device misinterprets ment or threshold rise.
the electrical interference as intrinsic rhythm. Whilst there are many similarities to the approach
In ICDs it may result in the delivery of shock taken with troubleshooting a permanent pacing sys-
therapy as the high frequency noise from tem, it is a more complex device and often will require
electrocautery may be interpreted as a tachycardia the assistance of a physician familiar with pacemak-
requiring treatment. ers. Pacing and sensing problems can originate in the
generator, the pacing leads, the lead– myocardium
interface or the patient. Table 10.2 lists the most fre-
Troubleshooting Pacing and ICD quent troubleshooting issues encountered in patients
Systems with pacemakers, their most frequent causes and rec-
Temporary pacing, either with epicardially or trans- ommendations to overcome the problem. Figure 10.2
venously placed leads, is often needed following car- illustrates ECGs of different pacemaker malfunctions.
diac surgery. Problems associated with temporary Most of the considerations made for pacemaker
pacing include the displacement of the lead, myo- troubleshooting are equally valid in patients with ICDs.
cardial perforation, which may lead to tamponade, Other important occurrences in these patients include
increasing pacing threshold, lack of capture and lack the delivery of inappropriate ICD shocks, ICD storms or
13:52:42 81
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(a) (b)
(c)
Figure 10.2 Pacemaker troubleshooting. (a) Failure to output (absence of pacing spikes causing a 3 second pause). (b) Failure to capture
(4th and 5th pacing spikes are not followed by ventricular electrograms). (c) Undersensing (all but the first pacing spike are delivered
inappropriately due to undersensing of electrical signals). (A black and white version of this figure will appear in some formats. For the colour
version, please refer to the plate section.)
ineffective ICD therapies in patients with true life-threat-

ening ventricular arrhythmias. As ICD systems are even
Cardioversion and Defibrillation in the
more complex than pacing systems, specialist input is Cardiothoracic Intensive Care Unit
invariably required in troubleshooting these devices. Defibrillation and cardioversion are occasionally
required in the CCU. Any atrial or ventricular tach-
Pacemaker and ICD ‘Magnet’ Mode yarrhythmia causing severe haemodynamic compro-
mise may need to be immediately dealt with using
Intensive care physicians should also be familiar with
electrical cardioversion and local advanced life sup-
the typical response of pacemakers and ICDs to mag-
port guidelines should be followed. Unsynchronised
net application but this should generally only be used
high energy shocks should be used to treat ventricular
when appropriate reprogramming of the device to the
fibrillation or very fast polymorphic VT, whereas syn-
desired function is not possible. Magnet modes can
chronised shocks should be used for cardioverting AF
vary between manufacturers and can permanently
and haemodynamically stable VT. Defibrillators deliv-
alter device function. Some new devices allow for pro-
ering biphasic waveforms should be preferably used.
gramming to ‘off ’ function.
Electrical cardioversion is very effective in the
A magnet placed over a pacemaker, but not an ICD,
treatment of tachyarrhythmias, but it should be
will usually make it pace in an asynchronous mode
borne in mind that unless the underlying cause of the
at a fixed heart rate. This is useful to protect pace-
arrhythmia is identified and treated, such as ischae-
maker dependent patients during diathermy or other
mia or electrolyte disturbance, there is a high prob-
sources of electromagnetic interference. However, not
ability of the arrhythmia recurring.
all pacemakers switch to a continuous asynchronous
mode when a magnet is applied, as the response to
magnet application may vary across models. Special Considerations for
Magnet application over an ICD will prevent the
device from sensing and delivering any therapies,
Defibrillation or Cardioversion
which is useful in patients having inappropriate ICD • Electrical cardioversion is contraindicated in
shocks or ICD storms or when electrocautery is being patients with known digitalis toxicity, not only
used. However, different ICD models may respond due to the lower efficacy in this context, but
differently, if at all, and in some cases therapies may also because junctional or paroxysmal atrial
be turned off completely until the magnet is removed tachycardia and even VF may occur within a few
and then reapplied. minutes of cardioversion.
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83
• Ipsilateral pneumothorax can increase pre-existing conduction system disease or history

defibrillation threshold in patients with an ICD of syncope and submitted to valve surgery.
and may result in unsuccessful defibrillation by • With any transvenous pacing system, intensive
the device. care physicians should be aware not only of any
• Patients with atrial fibrillation lasting for longer potential periprocedural complications, but also
than 24 to 48 hours and without appropriate issues such as the precautions required when
anticoagulation are at risk of stroke following performing direct current cardioversion, the
cardioversion and therefore this should not be utility of magnet application, electromagnetic
performed without previously excluding left atrial interference and apparent or real system
appendage thrombus with a transoesophageal malfunction with failure to pace, capture or sense
echocardiogram, unless there is significant and increasing pacing threshold.
haemodynamic compromise. Consideration • Appropriate management of an electrical storm
of anticoagulation should be made following includes the correction of the underlying cause,
cardioversion even in the absence of clots, the use of intravenous amiodarone or beta-
as the thromboembolic risk is higher in the blockers and reprogramming the ICD if the
postcardioversion period. arrhythmia is well tolerated. Magnet application
• When external cardioversion fails, potential may be useful to prevent subsequent therapies,
solutions include applying additional pressure while deep sedation or general anaesthesia may
to the paddles during the shock, changing the in some cases provide complete, albeit temporary,
electrodes to an anteroposterior orientation or control.
administering intravenous antiarrhythmics such • Electrical cardioversion is very effective in
as amiodarone (for both atrial and ventricular the treatment of tachyarrhythmias, but unless
arrhythmias) or ibutilide (for atrial fibrillation), the underlying cause of the arrhythmia is
which lower the energy required to restore sinus identified and treated there is a high probability
rhythm. of recurrence. When cardioversion fails,
applying additional pressure to the paddles
Conclusions during the shock, changing the electrodes to an
Cardiac arrhythmias and conduction disturbances are anteroposterior orientation or administering
frequent in the context of a cardiothoracic critical care intravenous antiarrhythmics which lower the
unit. Furthermore, an increasing number of patients energy required to restore sinus rhythm may be
with cardiac electronic devices are currently admitted useful.
to these units. It is imperative that the intensive care
physician is aware of the basic function of pacemak-
ers and implantable cardioverter-defibrillators, pos-
Further Reading
sible complications associated with the use of these Berdajs D, Schurr UP, Wagner A, et al. Incidence and
pathophysiology of atrioventricular block following
devices, the most frequent troubleshooting issues and mitral valve replacement and ring annuloplasty.
the diagnostic and therapeutic options that pacemak- European Journal of Cardiothoracic Surgery. 2008;
ers and ICDs may offer to critical patients. 34: 55–61.
Dawkins S, Hobson AR, Kalra PR, et al. Permanent
Learning Points pacemaker implantation after isolated aortic valve
replacement: incidence, indications, and predictors.
• In patients admitted to the cardiothoracic CCU
Annals of Thoracic Surgery. 2008; 85: 108–112.
and presenting with bradycardia, the decision
El-Chami MF, Sawaya FJ, Kilgo P, et al. Ventricular
to pace is based on the haemodynamic impact
arrhythmia after cardiac surgery: incidence, predictors,
caused by the underlying bradycardia, rather than and outcomes. Journal of the American College of
the specific rhythm disturbance per se. Cardiology. 2012; 60: 2664–2671.
• Recovery of severe conduction disturbances is Epstein AE, Di Marco JP, Ellenbogen KA, et al. ACC/
common in patients with sick sinus syndrome, AHA/HRS 2008 Guidelines for Device-Based Therapy
but unlikely in the case of complete heart block, of Cardiac Rhythm Abnormalities: a report of the
especially in patients at advanced age, with American College of Cardiology/American Heart
13:52:42 83
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84
Association Task Force on Practice Guidelines Merin O, Ilan M, Oren A, et al. Permanent pacemaker
(Writing Committee to Revise the ACC/AHA/NASPE implantation following cardiac surgery: indications
2002 Guideline) Journal of the American College of and long-term follow-up. Pacing and Clinical
Cardiology. 2008; 51: e1–62. Electrophysiology. 2009; 32: 7–12.
Erdogan HB, Kayalar N, Ardal H, et al. Risk factors for Mosseri M, Meir G, Lotan C, et al. Coronary pathology
requirement of permanent pacemaker implantation predicts conduction disturbances after coronary artery
after aortic valve replacement. Journal of Cardiac bypass grafting. Annals of Thoracic Surgery. 1991;
Surgery. 2006; 21: 211–215. 51: 248–252.
Glikson M, Dearani JA, Hyberger LK, et al. Indications, Nardi P, Pellegrino A, Scafuri A, et al. Permanent
effectiveness, and long-term dependency in permanent pacemaker implantation after isolated aortic valve
pacing after cardiac surgery. American Journal of replacement: incidence, risk factors and surgical
Cardiology. 1997; 80: 1309–1313. technical aspects. Journal of Cardiovascular Medicine
Gordon RS, Ivanov J, Cohen G, Ralph-Edwards (Hagerstown). 2010; 11: 14–19.
AL. Permanent cardiac pacing after a cardiac Onalan O, Crystal A, Lashevsky I, et al. Determinants of
operation: predicting the use of permanent pacemaker dependency after coronary and/or mitral
pacemakers. Annals of Thoracic Surgery. 1998; or aortic valve surgery with long-term follow-up.
66: 1698–1704. American Journal of Cardiology. 2008; 101: 203–208.
Knotzer H, Mayr A, Ulmer H, Lederer W. Reinelt P, Karth GD, Geppert A, Heinz G. Incidence and
Tachyarrhythmias in a surgical intensive care unit: a type of cardiac arrhythmias in critically ill patients: a
case-controlled epidemiologic study. Intensive Care single center experience in a medical-cardiological
Medicine. 2000; 26: 908–914. ICU. Intensive Care Medicine. 2001; 27: 1466–1473.
Liu Q, Kong AL, Chen R, et al. Propofol and Trappe H-J, Brandts B, Weismueller P. Arrhythmias in the
arrhythmias: two sides of the coin. Acta intensive care patient. Current Opinion in Critical Care.
Pharmacologica Sinica. 2011; 32: 817–823. 2003; 9: 345–355.
MCQs
1. In patients admitted to the cardiothoracic CCU fol- 3. In patients admitted to the cardiothoracic CCU and
lowing cardiac surgery, which features predict the presenting with a fast atrial arrhythmia, which acute
need for pacing in the event of significant bradycardia? measure should not be taken?
(a) Valve surgery rather than coronary (a) Direct current cardioversion in the case of severe
revascularisation haemodynamic compromise
(b) Advanced age (b) Unsynchronised direct current cardioversion
(c) History of syncope (c) Correction of any electrolyte disturbance
(d) Previous left bundle branch block (d) Administration of an appropriate antiarrhythmic
(e) All of the above medication, such as amiodarone, in the first hours
of well-tolerated atrial fibrillation
2. In patients admitted to the cardiothoracic CCU fol-
lowing cardiac surgery and with temporary pacing (e) Correction of underlying heart failure, myocardial
systems showing failure to capture, which underlying ischaemia, bleeding or anaemia
mechanisms should be considered? 4. A patient is day 1 post cardiac surgery and pac-
(a) Increase of the pacing threshold above ing dependent with epicardial temporary pacing
programmed value wires. Brief periods of asystole are seen on the moni-
tor. Which of the following measures should not be
(b) Lead displacement considered?
(c) Loose connections (a) Retesting the pacing threshold and increasing out-
(d) Hyperkalaemia, acidosis or alkalosis put if required
13:52:42
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85
(b) Checking the connectors of the pacing wires and (a) The atrium will be paced by the device
pacing box when needed
(c) Placement of transcutaneous pacing pads in case (b) The pacemaker will provide adequate AV
of need synchrony
(d) Increasing the sensitivity of the pacing system to (c) The pacemaker will prevent the heart from going
detect any intrinsic rhythm slower than 60 beats per minute
(e) Replacing the batteries in the pacing box (d) The pacemaker will be unaffected by the use of
5. A patient has a permanent pacemaker in situ in VVI electrocautery
mode and a lower heart rate limit of 60 beats per min- (e) The pacemaker will increase the patient’s heart rate
ute and is functioning normally. Which of the follow- beyond 60 beats per minute with exercise
ing statements is correct?
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Arterial and Venous Catheterisation and

Chapter
11 Invasive Monitoring
Stuart A Gillon, Nicholas A Barrett and Christopher IS Meadows
Principles of Vascular Access Table 11.1 Factors defining vascular catheters
Vascular catheters are ubiquitous to cardiothoracic Type of vessel: arterial, venous; peripheral, central
critical care. They may be defined or described on the Site of insertion: jugular, femoral, central, etc.
basis of numerous factors (Table 11.1). For the pur- Duration of access: short term, medium term, long term
poses of this chapter, vascular access relates to cath- Pathway from skin to vessel: tunnelled, non-tunnelled
eters within the arterial or central venous system. Length: short, mid, long
Additional features: number of lumens, antibiotic, antiseptic or
heparin impregnated
Insertion
Vascular catheter insertion within the critical care
unit is almost universally by the Seldinger technique:
a needle is inserted into the target vessel (or a tribu- Pressure Monitoring
tary of the target vessel); a guide wire is passed into
the vessel; one or more dilators are passed over the
Transducers
guide wire to create a tract through the skin and soft A transducer converts mechanical energy (hydrostatic
tissues; and the catheter is advanced over the guide pressure within the vascular system) into an electri-
wire, into the vessel. cal signal; the hydrostatic pressure within the cath-
Traditionally, the target vessel was sought using a eter is quantified and displayed as both a value and a
combination of anatomical landmarks and palpation. waveform.
The increasing availability of point-of-care ultrasound A continuous column of fluid maintains con-
technology within the critical care environment has tact between the transducer and the vascular sys-
led to a gradual move towards real-time ultrasound tem. Changes in pressure are transmitted down the
guided vascular access. The use of ultrasound for vas- column of fluid, leading to distortion of the trans-
cular access has been demonstrated to increase suc- ducer membrane. The membrane contains a strain
cess and reduce complications and is now considered gauge: distortion of the membrane stretches a wire,
a standard of care by the National Institute of Clinical altering its resistance. The wire is integrated into a
Excellence. Wheatstone bridge, which allows accurate determina-
Position may be confirmed by ensuring free aspi- tion of changes in resistance. The change in resistance
ration of blood, by transduction of pressure (thereby equates to change in pressure and this is displayed on
confirming arterial or venous placement), by meas- the monitor.
urement of the oxygen content of aspirated blood A valve within the transducer system permits
(suggestive of arterial or venous placement) or by flow of 3–4 ml of saline per hour through the arterial
imaging (either X-ray or ultrasound). line, to maintain line patency. Some units heparinise
the saline flush on the basis that this may reduce the
risk of intracatheter thrombus formation. The use of
Complications heparin, however, exposes the patient to heparin (and
The complications associated with line placement, associated reactions) and may interfere with the accu-
and potential strategies to minimise risk are listed in racy of coagulation samples drawn from the line if the
Table 11.2. flush fluid is incompletely removed prior to sampling.
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Chapter 11: Arterial and Venous Catheterisation
Table 11.2 Complications related to central venous catheter placement and strategies to reduce risk
Immediate Damage to adjacent structure (e.g. Ultrasound guidance, experienced operator (particularly in the presence of
arterial puncture, pneumothorax) anatomical abnormalities)
Air embolism Head-down position in jugular and subclavian approaches
Bleeding Correction of coagulopathy prior to insertion
Late Infection Introduction of CVC insertion ‘bundles’, full barrier precautions during insertion,
use of antibiotic impregnated catheters, use of antimicrobial impregnated patches
over the insertion site, avoidance of the femoral vein as an insertion site, removal
of catheters when no longer required
Thrombosis Avoidance of femoral insertion, use of heparin impregnated catheters, early
removal
Systematic review of studies examining the efficacy of is unaffected. Whilst pressure measurement systems
heparinised saline in this context found no convinc- are produced with material and dimensions most
ing evidence of improved catheter patency. suited to optimal damping, over-damping and under-
damping may occur.
Resonance and Damping
Every material has a natural frequency: the frequency Zeroing
at which it freely resonates. If a material is exposed Accurate measurement of physiological pressure
to a frequency close to its natural frequency it will requires the transducer to be ‘zeroed’ to atmospheric
resonate, or oscillate, at its maximum amplitude. This pressure (a system pressure of zero equates to atmos-
physical phenomenon is of significance to pressure pheric pressure, as physiological pressures are described
monitoring systems as, if the frequency of one of the as relative to atmospheric pressure). Calibration
components of the measured pressure wave is close to involves opening the pressure system to air, and refer-
the natural frequency, the excessive oscillation gener- encing this pressure to zero on the system. Transducers
ated will distort the measured pressure. are prone to baseline drift and therefore this process
In order to avoid this phenomenon, the natural should be undertaken several times per day.
frequency of a pressure monitoring system must be The height of the transducer relative to the patient
several orders of magnitude greater than the compo- is also important. By convention, the transducer
nent frequencies of the waveform being measured. should be at the same height above the floor as the
Using longer tubing, of wider diameter and using a left atrium of the patient. A transducer placed above
low density fluid within the tubing, will increase the or below the height of the atrium will lead to under-
natural frequency of a system. reading and over-reading of pressure respectively.
Damping describes the dissipation of energy in a
resonant, oscillating system. A pressure monitoring
system may be over-damped by tubing, which is of
Arterial Catheters
excessive length, insufficient diameter, or made from There are three major indications for placement of an
highly compliant material. Additionally, kinks, clots arterial catheter.
or air bubbles within the system will contribute to 1. Haemodynamic instability (either current or
damping. expected) in which beat to beat measurement
The optimal system strikes a balance between of arterial pressure allows close monitoring of
resonance and damping. A system with excessive haemodynamic state and safe titration of inotropic
resonance will tend to over-measure peak (systolic) and vasoactive drugs.
pressures and under-measure trough (diastolic) pres- 2. Need for frequent arterial blood sampling (e.g.
sures; mean pressure should be unaffected. Such sys- respiratory failure or severe, persistent metabolic
tems are described as under-damped. In contrast, a disturbance).
system with excessive damping and insufficient reso- 3. Non-pulsatile flow (for example in cardiac bypass
nance (damped system) will under-measure peak and or venoarterial ECMO) as there is no alternative
over-measure trough pressures; again mean pressure method of measuring systemic pressures.
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Arterial catheters may be inserted into: Pulse Pressure Variation

• Peripheral arteries (e.g. most commonly radial,
• The intrathoracic pressure varies throughout
also ulnar, brachial, dorsalis pedis);
the respiratory cycle; this alters the loading
• Central arteries (e.g. most commonly femoral,
conditions of the heart and results in variation
also axillary).
in stroke volume and pulse pressure between
The arterial pressure in peripheral arteries differs inspiration and expiration.
from that in central arteries. • The magnitude of this variation is greater
• A decrease in arterial compliance with increasing on the steep portion of the Frank–Starling
distance from the heart leads to a higher systolic curve (where a patient is likely to increase
and lower diastolic pressure measurement in cardiac output in response to fluid) than on
peripheral compared with central arteries; the the flat portion (with less likelihood of fluid
mean pressure should be comparable. responsiveness).
• The tone of peripheral arteries will demonstrate • Meta-analysis of studies relating to pulse
a more significant response to temperature and pressure variation (PPV) (and the closely
vasoactive medications than central arteries; related stroke volume variation) suggests that
measurement of peripheral arterial pressure variation of >13% is strongly predictive of fluid
could therefore be a poor reflection of the central responsiveness.
arterial pressure perfusing vital organs. • The studies relating to PPV were however largely
• These differences between central and peripheral conducted in highly controlled environments,
pressure are more pronounced in the elderly and in deeply sedated patients, with no spontaneous
in those with vascular disease. ventilation; analysis of the intensive care
population shows that few patients are
Information Derived from the Arterial comparable to the subjects of the initial studies;
Waveform the practical application of PPV in the clinical
setting therefore has significant limitations.
• Pulse rate
• Systolic blood pressure
• Diastolic blood pressure Central Venous Catheters
• Mean blood pressure A central venous catheter (CVC) is a vascular catheter
• The shape of the arterial waveform is determined with a tip sitting in the central venous system. These
by numerous factors: may be short catheters (15–20 cm) inserted into a
○ The stroke volume, central vein (femoral, jugular or subclavian) or longer
○ Left ventricular contractility, catheters inserted into a peripheral vein and advanced
○ Capacitance of the central arterial tree (the to the central circulation (peripherally inserted cen-
ability to distend and accommodate ejected tral catheter, PICC).
blood), Indications for CVC placement include the
○ Peripheral resistance (the rate at which blood following.
dissipates from the central arteries into • Administration of drugs which may only be
peripheral circulation). safely delivered directly into a central vein
• The dichrotic notch is the positive deflection in (e.g. amiodarone, noradrenaline, concentrated
the downstroke of the arterial waveform, which potassium, cytotoxic agents, total parenteral
represents closure of the aortic valve: nutrition).
○ Typically occurs at one third into the pressure • Measurement of central venous pressure
wave descent when aortic pressure (AoP) (CVP) or central venous oxygen saturation
exceeds left ventricular pressure (LVP); (ScvO2).
○ If peripheral resistance is reduced (e.g. sepsis), • To facilitate a procedure which requires access
AoP > LVP later in the cycle and the dicrotic to the central venous circulation (e.g. renal
notch shifts down the curve. replacement therapy, pulmonary artery catheter
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89
a not least because it is impossible to test in an intact

c
human circulation. It remains therefore primarily a
theoretical construct.
One key practical product of Guyton’s work has
v however arisen: the use of the RAP (in the form of
x CVP) in the clinical optimisation of cardiac output.
y
Guyton considered RAP to be an independent deter-
minant of SV (and therefore cardiac output). He pro-
Figure 11.1 CVP trace: a atrial contraction; c closure of tricuspid posed RAP and SV to have a similar relationship to
valve; x atrial relaxation; v ventricular contraction; y opening of the
tricuspid valve. that between end-diastolic volume and SV reported
by Starling. Given its ease of measurement, CVP was
thus widely integrated into clinical practice as a meas-
flotation, temporary pacing wire insertion, ure of left ventricular preload.
extracorporeal membrane oxygenation). The intervening six decades have witnessed sig-
• If peripheral venous access proves impossible. nificant technological advances in terms of haemody-
namic monitoring. Yet the use of CVP as a marker of
left ventricular preload persists. The Surviving Sepsis
Central Venous Pressure Trace Campaign, for example, recommends a CVP of 8–
The central venous pressure (CVP) trace is outlined 12 mmHg as a target for volume resuscitation in the
in Figure 11.1. shocked septic patient.
The clinical utility of CVP in the assessment of
Central Pressures preload is however questionable. Manipulation of
The CVP, when measured in the superior vena cava preload in the shocked patient is undertaken with a
(SVC) equates to right atrial pressure (RAP). The view to optimising cardiac output; any assessment of
significance of CVP in terms of the global haemody- preload is therefore beneficial only if it reliably iden-
namic state is complex and its role in management of tifies those patients in whom increase in preload
the haemodynamic state is controversial. (by fluid administration) is likely to increase car-
At the end of the nineteenth century, Otto Frank diac output. In clinical trials, the CVP has consist-
and Ernest Starling described the relationship between ently been shown to be a poor determinant of fluid
myocardial stretch and stroke volume and demon- responsiveness. As such, there are calls from some
strated an increase in cardiac output in response to quarters for the CVP as a marker of preload to be
increasing preload. This so- called Frank– Starling abandoned.
mechanism became a cornerstone of cardiovascu-
lar physiology and remains an important concept in Pulmonary Artery Catheter
haemodynamic management.
Some 50 years after this original work, Arthur History
Guyton built upon the Frank– Starling concept. The pulmonary artery catheter (PAC) evolved dur-
Guyton concluded, on the basis of a series of animal ing the twentieth century as a means of measuring
models, that venous return (Vr) was the key deter- pressure and flow within the pulmonary vasculature.
minant of cardiac output. According to the Guyton Ronald Bradley of St Thomas’ Hospital, London, first
model, Vr is determined by three factors: the mean described the placement of a catheter in the pulmo-
circulatory filling pressure (MCFP) (generated by the nary circulation of humans in the 1950s. This origi-
elastic properties of the vasculature and the hydro- nal catheter was, however, difficult to site. Harold
static force exerted by volume within the vessels, the Swan (an alumnus of St Thomas’ Medical School) and
so-called stressed volume); RAP (against which the his colleague William Ganz (Cedars-Sinai Medical
MCFP must drive); and the venous resistance (which Center, Los Angeles) adapted Bradley’s design by
may be altered by changes in regional blood flow to adding a flotation balloon, thereby enhancing ease
organ vascular beds). The accuracy of this complex of insertion. The names of Swan and Ganz have since
model remains the subject of significant debate, become eponymous with the PAC.
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Components 40
• A typical adult PAC is 110 cm in length and 7–8 F Right Right Pulmonary Pulmonary artery
atrium ventricle artery wedge
in diameter; distance markers are found every
10 cm to guide insertion. 30
• It is made of radio-opaque polyvinyl chloride.
Pressure (mmHg)
• There are typically four lumens, the most distal
is located at the tip and used for measuring 20
pulmonary pressures; the most proximal is
located around 30 cm from the tip, measures RAP
and serves as the route of injection of cold saline
for cardiac output measurement. 10
• A thermistor is located close to the tip for the

purposes of cardiac output and core temperature
measurement. 0
• A balloon, 1–1.5 ml in volume, is located close
Figure 11.2 Pulmonary artery catheter waveform as it is ‘floated’
to the tip of the catheter; this is inflated for the through the heart into pulmonary circulation.
purposes of flotation into the pulmonary artery,
and measurement of the pulmonary artery wedge
pressure.
smooth motion; the passage of the catheter from
Indications atrium to ventricle to pulmonary artery may be
tracked by:
Indications for insertion of the PAC include:
○ The changing pressure waveform
• Cardiac output monitoring;
(Figure 11.2), the most common approach;
• Measurement of right heart pressures, pulmonary
○ Fluoroscopy;
artery pressure, and left atrial pressure;
○ Transoesophageal echocardiography.
• Measurement of central venous oxygen saturation
(ScvO2) and mixed venous oxygen saturation
(SvO2). Pulmonary Artery Measurements
The PAC allows measurement of pressure and flow
within the pulmonary vasculature. Table 11.3 outlines
Insertion of the Pulmonary Artery direct and indirect variables, which may be obtained
Catheter from the PAC.
• The procedure is undertaken using an aseptic
technique; all lumens of the catheter are flushed; Cardiac Output Monitoring
the distal port is connected to a pressure The PAC measures cardiac output by means of ther-
transducer. modilution. A known volume of cold saline is rapidly
• An insertion sheath is placed using a Seldinger injected into the proximal, RA, port. The resultant
technique into a central vein (right internal change in temperature of blood is measured by the
jugular and left subclavian provide the most thermistor at the tip of the PAC and a washout curve
direct route for the flotation catheter). is generated. Blood flow, which equates to cardiac
• The PAC is introduced via the sheath; once the tip output, is inversely proportional to the rate of tem-
is sitting within the vena cava or right atrium, the perature change; flow is quantified by means of the
balloon is inflated and the catheter advanced in a Stewart–Hamilton equation:
k(core temperature − indicator temperature)

volume of indiicator
CO =
Change in blood temperature
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Table 11.3 Direct and indirect variables obtained from the pulmonary artery catheter
Variable Equation Normal values

Direct measurements Right atrial pressure (RAP) 2–6 mmHg
Right ventricular pressures (RVP) systolic 20–30 mmHg
diastolic 0–5 mmHg
Pulmonary artery pressures (PAP) systolic 20–30 mmHg
diastolic 8–12 mmHg
mean 10–20 mmHg
Pulmonary artery wedge pressure (PAWP) 4–12 mmHg
Cardiac output (CO) 4–8 l/min
Derived variables Cardiac index (CI) CO 2.5–4 l/min
BSA
Systemic vascular resistance (SVR) MAP − RAP 800–1200 dyne s/cm5
CO
Pulmonary vascular resistance (PVR) mPAP − PAWP 37–250 dyne s/cm5
CO
DO2 CO ( SpO2 × Hb × 1.34) + (0.003PaO2 )
VO2 10 (CaO2 − CvO2 ) × CO
where k is a constant. The appropriateness of the randomised control

The traditional means of cardiac output monitor- trial as a means of testing a monitoring tool is however
ing via the PAC relies upon intermittent bolus stud- questionable, since the utility of the PAC is dependent
ies and cannot therefore provide continuous cardiac upon clinician ability to correctly interpret the results.
output monitoring. Variants of the PAC are now avail- Therefore, whilst there have been calls to remove the
able which have a heating element in the region of the PAC from clinical practice based upon the results of
proximal injection port. This element intermittently the above named trials, the PAC proponents remain,
heats the passing blood, allowing regular washout particularly amongst those clinicians managing com-
curves to be created and near-continuous cardiac out- plex cardiac patients.
put to be calculated.
Transpulmonary Dilution and Pulse
Evidence Basis Contour Analysis
The PAWP may be used in a similar manner to the CVP,
as a static marker of preload. However, like the CVP, the PiCCO
PAWP has been demonstrated to be a poor predictor of
• The PiCCO system utilises a modified arterial
fluid responsiveness and has therefore, in many centres,
line to provide advanced cardiovascular
been replaced by other, dynamic assessments.
monitoring.
The impact of PAC monitoring upon outcome has
• The PiCCO arterial line is inserted in a central
been tested in randomised control trials in the gen-
artery (usually femoral, alternatively axillary).
eral intensive care population (PACMAN study), in
• The PiCCO connects to a transducer, providing
patients admitted with acute respiratory distress syn-
standard arterial line information.
drome (ARDSnet group), in high risk cardiac surgical
patients and those with severe heart failure (ESCAPE • A thermistor, at the tip of the PiCCO line,
study). No study demonstrated improved outcomes allows performance of transpulmonary
with the additional information provided by the PAC thermodilution.
and there was an increased incidence of adverse, cath- ○ 15 ml of cold saline is injected into a
eter related, events. central line placed in the internal jugular or
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subclavian vein; a sensor placed in the CVC muscle relaxants (which cross react with the
port monitors the timing of injection and the molecular sensor).
temperature of the injectate. ○ The lithium injectate does not require a CVC;
○ The cold injectate crosses the pulmonary a peripheral cannula will suffice.
circulation and enters the systemic ○ LiDCO does not provide the volumetric
circulation; the resultant change in blood measurements offered by the PiCCO.
temperature is monitored by the PiCCO
thermistor; a temperature washout
curve –similar to that generated by a Non-calibrated Systems
PAC –is used to determine cardiac In addition to the PiCCO and LiDCO, several non-
output. calibrated systems are available. Like the continu-
○ PiCCO transpulmonary thermodilution also ous cardiac output monitoring offered by calibrated
provides volumetric data. counterparts, these non- calibrated systems utilise
■ Global end diastolic volume (index) waveform analysis to determine stroke volume and
(GEDVI) (650–1000 ml/m2), volume of subsequently cardiac output. They may offer stroke
blood within the cardiac chambers at end- volume variation (as described in the arterial wave-
diastole; indicative of preload. Typically form section). The lack of calibration has called the
indexed to body surface area. accuracy of these systems into question and compari-
■ Intrathoracic blood volume (index) son to calibrated systems demonstrates a discrepancy
(ITBVI) (800–1000 ml/m2), volume of between measured cardiac output.
blood within the chest, derived from
thermodilution technique; indicative of
preload.
Learning Points
• Vascular access is a common undertaking in
■ Extravascular lung water (index)
critical care; the use of insertion bundles and real-
(EVLWI) (3–7 ml/m2), volume of
time ultrasound appears to reduce the incidence
water lying within the lung
of complications.
parenchyma, a marker of pulmonary
• Central venous pressure appears to be a poor
oedema.
predictor of fluid responsiveness in clinical
• Following calibration using the described
practice, it may however offer information
thermodilution technique, the PiCCO
regarding the venous system not obtainable by
system uses mathematical analysis of the
other means.
pulse waveform to provide continuous
• The pulmonary artery catheter offers a means of
measurement of stroke volume (and therefore
measuring pulmonary pressures, cardiac output
cardiac output).
and a surrogate of left atrial pressure; its use has
not however been demonstrated to change patient
LiDCO outcomes.
• The LiDCO, like the PiCCO, utilises a • Transpulmonary thermodilution and pulse
transpulmonary dilutional technique to contour analysis techniques are more commonly
determine cardiac output. There are however a employed means of measuring cardiac output
number of differences. than the pulmonary artery catheter; performance
○ The LiDCO utilises a standard arterial line, in trials is comparable to the pulmonary artery
in any artery; the LiDCO system is attached catheter.
externally to the arterial line. • Dynamic markers of cardiovascular performance,
○ Lithium is used for the dilution technique, such as pulse pressure analysis, may be more
rather than cold saline; the dependence accurate in determining volume status than
upon lithium makes the LiDCO unreliable traditional static parameters; whether this
in those patients on therapeutic lithium or accuracy is maintained in the complex critical
who have recently received non-depolarising care population is not clear.
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Further Reading McGee DC, Gould MK. Preventing complications of

central venous catheterization. New England Journal of
Binanay C, Califf R, Hasselblad V, et al. Evaluation study Medicine. 2003; 348: 1123–1133.
of congestive heart failure and pulmonary artery Pronovost P, Needham D, Berenholtz S, et al. An
catheterization effectiveness: the ESCAPE trial. intervention to decrease catheter-related bloodstream
Journal of the American Medical Association. 2005; infections in the ICU. New England Journal of
294: 1625–1633. Medicine. 2006; 355: 2725–2732.
Guyton AC. Determination of cardiac output by equating Sakka S, Kozieras J, Thuemer O, van Hout N. Measurement
venous return curves with cardiac response curves. of cardiac output: a comparison between
Physiological Reviews. 1955: 35: 123–129. transpulmonary thermodilution and uncalibrated
Harvey S, Harrison DA, Singer M, et al. Assessment of the pulse contour analysis. British Journal of Anaesthesia.
clinical effectiveness of pulmonary artery catheters 2007; 99: 337–342.
in management of patients in intensive care (PAC- Sandham JD, Hull RD, Brant RF, et al. A randomized,
Man): a randomised controlled trial. Lancet. 2005; controlled trial of the use of pulmonary-artery
366: 472–477. catheters in high-risk surgical patients. New England
Marik PE, Cavallazzi R. Does the central venous pressure Journal of Medicine. 2003; 348: 5–14.
predict fluid responsiveness? An updated meta- Wheeler A, Bernard G, Thompson B, et al. Pulmonary-
analysis and a plea for some common sense. Critical artery versus central
Care Medicine. 2013; 41: 1774–1781. venous catheter to guide treatment of acute lung
Marik PE, Lemson J. Fluid responsiveness: an evolution injury. New England Journal of Medicine. 2006;
of our understanding. British Journal of Anaesthesia. 354: 2213–2224.
2014; 112: 617–620.
MCQs
1. What degree of pulse pressure variation is suggestive (d) Antimicrobial impregnated patch over
of fluid responsiveness? insertion site
(a) >5% (e) Introduction of an insertion ‘bundle’ into the
department
(b) <5%
4. At which point in the cardiac cycle does the dichrotic
(c) >13% notch occur?
(d) <13% (a) End systole
(e) >100% (b) Mid systole
2. Which of the following parameters is derived from (c) End diastole
pulmonary artery catheter measurements? (d) Mid diastole
(a) Cardiac output (e) None of the above
(b) Systolic pulmonary artery pressure 5. Which of the following pulmonary artery catheter
(c) Pulmonary artery wedge pressure measurements is most in keeping with a patient with
cardiogenic shock secondary to an anterior myocar-
(d) Pulmonary vascular resistance dial infarction?
(e) Right atrial pressure (a) Cardiac index 1.6 l/min/m2; pulmonary artery
3. Which of the following is NOT associated with wedge pressure 22 mmHg; mean pulmonary
decreased incidence of central line associated artery pressure 27 mmHg; central venous oxygen
infection? saturation 44%
(a) Full barrier precautions at time of insertion (b) Cardiac index 1.6 l/min/m2; pulmonary artery
wedge pressure 4 mmHg; mean pulmonary
(b) Early removal of central line artery pressure 10 mmHg; central venous oxygen
(c) Insertion into the femoral vein saturation 44%
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(c) Cardiac index 4.6 l/min/m2; pulmonary artery artery pressure 14 mmHg; central venous oxygen
wedge pressure 8 mmHg; mean pulmonary saturation 64%
artery pressure 12 mmHg; central venous oxygen (e) Cardiac index 2.2 l/min/m2; pulmonary artery
saturation 84% wedge pressure 12 mmHg; mean pulmonary
(d) Cardiac index 2.6 l/min/m2; pulmonary artery artery pressure 36 mmHg; central venous oxygen
wedge pressure 9 mmHg; mean pulmonary saturation 64%
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Section 3 Therapeutic Intervention
Antibiotics in the Cardiothoracic Intensive

Chapter
12 Care Unit
Oana Cole and Olly Allen
The modern era of antibiotics starts with the dis- the median length of stay and the hospital mortal-
covery of penicillin by Alexander Fleming in 1928. ity were significantly higher in the inappropriate
Since then, antibiotics have transformed the face of antibiotic group.
modern medicine and enabled major advances in An example of an algorithm for presumptive anti-
the treatment of patients. So much so that antibiotics biotic therapy for pneumonia in a critically ill patient
could partially be credited for the staggering increase is presented in Figure 12.2.
in the general population’s life expectancy from Critically ill patients have multiple risk factors
around 60 years old in the UK in the 1920s, accord- for serious and life-threatening infections. Exposure
ing to the Office for National Statistics, to 81 years to antibiotics and other treatments which eradicate
old in 2015. and modify the commensal flora, compromised host
Critical care is a young specialty whose evolution defences due to nutritional deficiencies, critical illness,
has largely been shaped by the evolution of antimicro- compromised integument (intravascular devices, per-
bial therapy. It can be argued that the only treatment cutaneous interventions and devices) and disruption
we can offer our patients is antimicrobials, the rest – of cellular and humoral immunity as in the transplant
vasoactive medications, mechanical ventilation, diu- patients lead to a high susceptibility to sepsis. In the
retics and so on –are merely supportive measures. context of severe infections, Table 12.1 highlights the
The aim of this chapter is to present the aspects most prevalent microorganisms in Western world
of antimicrobial therapy most pertaining to a cardio- critical care patients.
thoracic critical care context. Data are presented as
valid in 2016. We do not assume to give an exhaust-
ive representation of the myriad of issues faced by the Antibiotic Administration in the
modern intensivist, but to offer a brief update of the Critically Ill Patient
most important issues we are currently confronting. In the last few years there has been a focus on the most
appropriate way of administering and dosing antibi-
‘Appropriate’ Antibiotic Therapy otics in intensive care. This has been triggered by a
There is no universal recipe for which antibiotics better understanding of the critical illness pathophysi-
should be used first in a critically ill patient. As shown ology, as well as the emergence of new technologies
in Figure 12.1, the choice is individualised for the that alter the pharmacodynamics and pharmacokin-
patient, unit, hospital and geographical area. Most etics of drugs in this patient population (Figure 12.3).
clinicians, when faced with a patient with a severe Time dependent antimicrobials (fT>MIC) include
infection or septic shock, would choose to start with beta-lactams, glycopeptides, macrolides and linezolid.
a broad spectrum antibiotic or combination and nar- Their concentrations have to be well above the mini-
row down as pathogens and their susceptibilities are mum inhibitory concentration (MIC) for the pathogen
identified. for at least 40% of the interval between doses in order
The comparative effects of appropriate and to achieve their therapeutic targets. There is a grow-
inappropriate antibiotic therapy are well illustrated ing body of research concerning the administration of
in a recent retrospective study by Neinaber et al. beta-lactams as a continuous or prolonged infusion so
conducted over 6 years in a single institution in the that the optimum concentration is achieved for sus-
USA. In this study, the risk of nosocomial infections, tained periods of time.
13:57:49 95
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Section 3: Therapeutic Intervention
ANTIBIOTIC
CHOICE
LABORATORY-
EMPIRICAL
GUIDED
Consultation
Individual case Efficacy in Cost-benefit Susceptibility
Policy/protocol with
advice clinical studies ratio report
microbiologist
Known
Evidence based
Clinical Knowledge of sensitivity and
on hospital and
suspicion likely cause resistance of
national trends
local flora
Figure 12.1 Flow chart for choice of antibiotic.
No Follow CAP
guidelines
Concern for
No Vancomycin
HCAP?
PLUS
antipseudomonal
Yes beta-lactam
OR
carbapenem +/–
vancomycin
Currently
mechanically
Vancomycin
ventilated?
PLUS
antipseudomonal
No beta-lactam
OR
carbapenem +/–
vancomycin
concern for
Yes HAP or VAP
MDRs? Carbapenem OR
antipseudomonal
beta-lactam PLUS
+/– vancomycin
(or linezolid) PLUS
Yes aminoglycoside
OR
antipseudomonal
fluoroquinolone
PLUS
vancomycin
Figure 12.2 Presumptive antibiotic therapy for pneumonia in the ICU. HCAP Health Care Associated Pneumonia; HAP hospital acquired
pneumonia.
Concentration dependent antimicrobials (fCmax/ The antibiotic concentrations in the target tissues
MIC) include aminoglycosides, fluoroquinolones, are influenced by the pharmacokinetic changes in the
metronidazole, echinocandins, polyenes and dapto- critically ill patient.
mycin. These antibiotics need to be administered in 1. Volume of distribution, Vd –increased for
doses which achieve target concentrations well above hydrophilic drugs due to increased total body
8–9 times MIC of the pathogen. water; unchanged for lipophilic drugs.
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Chapter 12: Antibiotics
Table 12.1 Most prevalent organisms in Western world critical care patients
Diagnosis Potential pathogens Initial therapy Alternative therapy

Catheter-related blood S. aureus, coagulase- Flucloxacillin Vancomycin
stream infections negative staphylococci, Vancomycin Linezolid
Gram-negative rods Tazocin Ciprofloxacin
Candida spp. Fluconazole Echinocandins
Infectious endocarditis Streptococci, Amoxicillin Flucloxacillin – MSSA
S. aureus, Enterococci Flucloxacillin Vancomycin – MRSA
Vancomycin Gentamicin if Enterococci
± gentamicin Rifampicin if prosthetic valve
± rifampicin
Pneumonia, including VAP Gram-negative rods, Piperacillin-tazobactam Carbapenems
Haemophilus, S. pneumoniae Ciprofloxacin
Penicillins
Sepsis/bacteraemia S. aureus, Gram-negative rods Piperacillin-tazobactam Fluoroquinolone
Candida spp. Flucoxacillin Vancomycin
Aspergillus Vancomycin Echinocandins
Fluconazole Amphotericin B
Voriconazole Echinocandins
Figure 12.3 The kill characteristics of antibiotics.

Modified from Tsai et al. (2015).
f Cmax/MIC
E.g. aminoglycosides
Drug concentration
fAUC0–24:MIC
E.g. glycopeptides
4x MIC
MIC
Time
f T>MIC
f T>4XMIC E.g. β-lactams
2. Clearance and elimination –may change elimination half-time and the risk of toxicity and
according to the renal and hepatic blood flows drug accumulation.
and function; severely deranged in septic shock; 5. Tissue penetration –can be variable due to
drug clearance and elimination also dependent on microcirculatory dysfunction.
whether renal replacement therapy is instituted.
3. Decreased albumin levels –the volume of Special Case –Antibiotics and
distribution and clearance of protein-bound drugs Extracorporeal Circuits
increase, decreasing their efficacy. The pharmacokinetics of antibiotics in patients on
4. End-organ dysfunction –cardiac dysfunction extracorporeal circuits is a growing area of research.
in the context of septic shock increases the The volume and distribution and clearance of drugs
13:57:49 97
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98
24 Figure 12.4 Meropenem concentration

during ECMO run with two different dosing
regimens.
20
Meropenem concentration (mg/l)
16
12
Target concentration (8 mg/l)

8
0
0 4 8 12
Time (h)
Standard dosing (1g/8 h) High-dose infusion (6.5 g/24 h)
is altered and these are compounded by the added includes transcatheter implanted valves and
potential for sequestration in the circuit. The import- homografts.
ance of understanding the pharmacology and chan- 2. Patients with previous IE; they also have a higher
ging the doses and intervals of administration of risk of infectious complications than patients with
antimicrobials is colossal, since subtherapeutic doses a first episode of IE.
are associated with worse outcomes. 3. Patients with untreated cyanotic congenital
An example is provided in Figure 12.4, which heart disease (CHD) or with prosthetic baffles
shows the effect of two dosing regimens of merope- or conduits as part of palliative management;
nem, as described by Shekar et al. (2013). the European Society of Cardiology (ESC)
Unfortunately, data are very limited to be able to guidelines 2015 recommend that patients with
generalise these results for all antimicrobials. What is definitive repair of CHD with prosthetic material
certain, though, so far, is that ‘one size does not fit all’ should only receive antibiotic prophylaxis for the
when it comes to drug dosing in patients on extracor- first 6 months, while endothelialisation of the
poreal circuits. If feasible, drug levels should be moni- prosthetic material occurs.
tored in this category of patients in order to establish
Diagnosis of infective endocarditis is based on the
the appropriate therapeutic regime.
modified Duke criteria and the ESC 2015 guidelines,
as shown in Table 12.2.
Endocarditis and Intracardiac Device Successful treatment of IE involves primarily
Infection pathogen eradication. Surgical treatment and the
treatment of complications are beyond the scope of
Infective endocarditis (IE) is a deadly disease. Despite
this chapter. With respect to antimicrobials in IE,
major improvements in diagnosis and treatment, IE
there are currently the following recommendations,
remains associated with high morbidity and mortal-
according to the British Society of Antimicrobial
ity. IE patients admitted to critical care are among the
Chemotherapy, 2012 guidelines.
sickest the intensivist will have to deal with.
The following categories of patients have the high- 1. Initial empirical treatment of native valve
est risk to acquire IE, as well as a poorer prognosis of endocarditis (NVE) depends on the clinical
the disease: presentation.
1. Patients with a prosthetic valve or with prosthetic (i) NVE indolent presentation: amoxicillin +
material used for valve repair; this category gentamicin.
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Table 12.2 Diagnosis of infective endocarditis
Definite IE
Pathological criteria • Positive blood cultures for IE
• Microorganisms identified on histological analysis of vegetation or embolic material
• Vegetation or embolic material identified by histology
Clinical criteria • 2 major criteria
• 1 major criterion and 3 minor criteria
• 5 minor criteria
Possible IE
• 1 major criterion and 1 minor criterion
• 3 minor criteria
Unlikely/rejected IE
• Firm alternative diagnosis
• Resolution of symptoms with antibiotic treatment ≤4 days
• No histological evidence of IE
Major and minor criteria of IE (ESC, 2015)

Major criteria
Blood cultures positive
Typical IE microorganisms from 2 separate cultures
Viridans streptococci, Streptococcus gallolyticus (Streptococcus bovis), HACEK group, Staphylococcus aureus; or
Community acquired enterococci in the absence of a primary focus; or
Microorganisms consistent with IE from persistently positive blood cultures:
≥2 positive blood culture drawn >12 hours apart; or
All 3 or a majority of ≥4 separate blood cultures (with first and last sample drawn >1 hour apart); or
Single positive blood culture for Coxiella burnetii or phase I IgG antibody titre >1:800
Imaging positive for IE
Echocardiogram positive for IE
Vegetation
Abscess, pseudoaneurysm or intracardiac fistula
Valvular perforation or aneurysm
New partial dehiscence of prosthetic valve
Abnormal activity around the site of prosthetic valvular implantation detected by radiolabelled WBC SPECT/C T
Definite paravalvular lesions by cardiac CT
Minor criteria
Predisposition –heart condition or intravenous drug administration
Temperature >38 °C
Vascular phenomena: major arterial emboli, septic pulmonary infarcts, intracranial haemorrhage, conjunctival
haemorrhages and Janeway’s lesions
Immunological phenomena –glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor
Microbiological evidence –positive blood culture but does not meet the major criteria above or serological
evidence of active infection with a microorganism consistent with IE
(ii) NVE severe sepsis: vancomycin + gentamicin. 3. Antibiotic treatment of IE due to oral streptococci
(iii) NVE severe sepsis + risk of MDR: and Streptococcus bovis group depends on
vancomycin + meropenem. minimum inhibitory concentration, MIC (usual
2. Prosthetic valve endocarditis (PVE): vancomycin course is 4 weeks for NVE and 6 weeks for PVE).
+ gentamicin + rifampicin; this applies to all PVE (i) Penicillin-susceptible strains, non-penicillin
irrespective of time. allergic patients:
13:57:49 99
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100
(a) Benzylpenicillin, or (iii) Multiresistance to beta-lactams,

(b) Amoxicillin, or aminoglycosides and vancomycin:
(c) Ceftriaxone. (a) Daptomycin and ampicillin,
(ii) Penicillin-susceptible strains, penicillin- (b) Linezolid,
allergic patients: Vancomycin BD. (c) Vancomycin, if beta-lactam resistance
(iii) Strains relatively resistant to penicillin but vancomycin susceptibility detected.
(higher MIC required), non-penicillin We must stress that these are only guidelines, and
allergic patients: that individual hospitals in different regions may have
(a) Benzylpenicillin, double the dose different antibiotic policies, depending on the local
for penicillin-susceptible strains and ecology.
gentamicin, or
(b) Amoxicillin, double the dose for
penicillin-susceptible strains and
Catheter Related Bloodstream
gentamicin, or Infections
(c) Ceftriaxone and gentamicin. The definition of catheter related bloodstream infec-
(iv) Strains relatively resistant to penicillin tions, also known as central line associated blood-
(higher MIC required), penicillin- stream infections (CLABSI), is bacteraemia or
allergic patients: Vancomycin and fungaemia in a patient with an intravascular catheter,
gentamicin. sepsis and at least one positive blood culture taken
4. Antibiotic treatment of IE due to Staphylococcus from a peripheral vein, in the absence of another
spp., for NVE: apparent source except for the catheter. In add-
(i) Methicillin-susceptible Staphylococcus spp., ition, there should be evidence that the catheter was
non-penicillin-allergic patients: infected based on quantitative or semi-quantitative
methods. Another diagnostic method for CLABSI is
Flucloxacillin. differential time to positivity –blood cultures taken
(ii) Methicillin-susceptible Staphylococcus from the central line presumed to be infected may
aureus, alternative strategy: turn positive at least 2 hours before blood cultures
Vancomycin or daptomycin. taken simultaneously from a peripheral vein. This is
(iii) Penicillin-allergic patients or methicillin- due to the almost three-fold increase in the micro-
resistant Staphylococcus spp.: organism load of an infected catheter compared to
(a) Vancomycin for 4–6 weeks, intravenous blood.
administration, Prevention of CLABSI relies on several measures,
(b) Daptomycin for 4–6 weeks, intravenous as follows:
administration. 1. Choice of insertion site –femoral lines should
5. Antibiotic treatment of IE due to Enterococcus be a last resort; they should be changed as soon
spp.: as possible, within a maximum time frame of
(i) Beta-lactam and gentamicin-susceptible 48 hours.
strains: 2. Insertion techniques –experienced personnel,
(a) Amoxicillin and gentamicin for 4 avoidance of haematoma formation around the
weeks for NVE or 6 weeks for PVE, insertion site.
(b) Ampicillin with ceftriaxone for 4 3. Adoption of a care bundle; the Matching Michigan
weeks for NVE or 6 weeks for PVE, for campaign has shown that CLABSI decreased by
E. faecalis, more than 60% over 2 years in ICUs in England
(c) Vancomycin and gentamicin for 6 after introduction of a care bundle.
weeks if penicillin allergy known or 4. Antibiotic-coated central venous catheters have
suspected. been proposed and adopted with success across
(ii) Gentamicin-resistant species – replace intensive care units worldwide. The catheters are
gentamicin with streptomycin, if susceptible impregnated with minocycline-rifampicin and
to the latter. are effective in inhibiting the development of
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Table 12.3 Systemic treatment of CLABSI –a possible guide
Pathogen First line antibiotic Alternative treatment

Coagulase-negative staphylococci
Methicillin-sensitive Flucloxacillin mecA gene negative Vancomycin
Methicillin-resistant Vancomycin Daptomycin or linezolid
S. aureus
MSSA Flucloxacillin Vancomycin
MRSA Vancomycin Daptomycin or linezolid
Enterobacteriaceae
ESBL –ve Piperacillin/tazobactam Ciprofloxacin or aztreonam
ESBL +ve Carbapenem Ciprofloxacin
Pseudomonas Carbapenem or piperacillin-tazobactam Ciprofloxacin or aztreonam
May consider the addition of an aminoglycoside
Candida spp. Echinocandins or fluconazole Amphotericin
Candida glabrata Echinocandins or fluconazole at higher Amphotericin
doses if susceptible strains
Table 12.4 Retrospective analysis of all VAD patients from the Mayo Clinic between 2005 and 2011
Infection type Cases per 100 patient-years of LVAD support (95% CI)
All 32.8 (26.7–39.9)
Endocarditis 1.6 (0.5–3.8)
Pump and/or cannula infection 4.9 (2.7–8.0)
Bloodstream infection
VAD related 7.5 (4.7–11.2)
Non-VAD related 6.8 (4.2–10.4)
CLABSI related 3.3 (1.6–6)
CLABSI associated 1.6 (0.5–3.8)
Pocket infection 2.3 (0.9–4.7)
Driveline infection 15 (10.9–20)
Permanent pacemaker/CRT-D infection 1.6 (0.5–3.8)
Mediastinitis, VAD related 2 (0.7–4.2)
biofilm of both Gram-negative and Gram-positive a percutaneous drive-line, which has been termed
bacteria, with the exception of P. aeruginosa and the ‘Achilles’ heel’ of these devices. The most recent
Candida spp. INTERMACS report (March 2016) has shown that
major infections in MCSD are the third highest cause
Table 12.3 shows possible systemic treatment for
of death with an overall death toll of 9% (June 2006 to
CLABSI.
March 2016), surpassed only by neurological dysfunc-
tion and multiorgan failure.
Mechanical Circulatory Support Device The results of a retrospective analysis of all VAD
(MCSD) Infections patients from the Mayo Clinic between 2005 and 2011
Infections in MCSD patients are difficult to treat are shown in Table 12.4.
and have been associated with poor prognosis and The salient points of international standards for
poor quality of life. Ventricular assist devices differ the management of MCSD infections as valid in June
from other cardiac devices by the fact that they have 2016 are presented below.
13:57:49 101
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1. Bacterial infections: infections in intensive care is increasing due to the

(a) Gram-positive cocci are the most prevalent increasing complexity of medical and surgical ICU
pathogens, followed by Gram-negative rods. patients, the presence of medium-and long- term
(b) Nosocomial pathogens – Pseudomonas, devices, such as ECMO and VAD cannulae, and the
Serratia and Enterobacter –account for use of broad spectrum antibiotics.
the second most common cause after Although all species of yeasts can be encoun-
Staphylococcus spp. tered, Candida and Aspergillus spp. are by far the
(c) The duration of antimicrobial treatment is not most prevalent in cardiothoracic ICU patients, so we
clearly established; most centres recommend will refer to treatment for these two pathogens in the
courses of at least 2 weeks for superficial discussion below.
driveline infections and at least 4 weeks for 1. Candida spp:
deep-seated infections.
(a) The 2012 European guidelines recommend
(d) Due to the wide variety of possible scenarios, that fungicidal agents –echinocandins or
there are currently no international guidelines lipid-based polyenes –be used for the initial
on the treatment of bacterial infections treatment of invasive Candida infection; once
associated with MCSD. The antibiotic agents the species of Candida and the sensitivities are
should be administered after consultation with identified, treatment can be de-escalated to
the local microbiology department, infectious azoles for susceptible strains.
diseases specialist and the transplant or heart
(b) Polyenes are preferred to other classes for the
failure specialist teams.
treatment of deep-seated infections, such as
2. Fungal infections:
mediastinitis or endocarditis.
(a) The prevalence of fungal infections has
2. Aspergillus:
increased over the years.
(b) Most fungal infections are caused by (a) Caspofungin is the only echinocandin
Candida spp., with a few other case reports of approved for the treatment of invasive
Aspergillus spp. and other yeasts. aspergillosis; however, it is an inferior choice
to voriconazole and amphotericin.
(c) No evidence has demonstrated that the
routine use of antifungal prophylaxis (b) Voriconazole is recommended as first line
decreases the rate of fungal infections in agent for aspergillosis; notably, it interacts
MCSD patients; however, preimplantation with tacrolimus and cyclosporine by
prophylaxis should be considered in high-risk interfering with the hepatic metabolism
patients. pathways; the therapeutic levels of the
immunosuppressants should be monitored
(d) Candida spp. pump or cannula infection
and higher doses may be required.
should be treated with 8–12 weeks of
amphotericin, echinocandin intravenously or (c) Lipid-based polyenes (amphotericin B)
high dose fluconazole if susceptible Candida are recommended as second line therapy
strains. for aspergillosis, where voriconazole is
contraindicated.
(e) Deep-seated pocket or driveline infection
should be treated with 8–12 weeks of
echinocandin or amphotericin intravenously Antibiotic Resistance and the
followed by prolonged suppressive oral Development of New Agents
therapy. The last decade has seen worrying levels of increased
(f) Superficial driveline infections should be antimicrobial resistance, prompting the Centre for
treated with 2 weeks of azole therapy. Disease Control in the USA and similar organisations
worldwide to declare the current situation an emer-
Antifungals in the ICU gency. The Review of Antimicrobial Resistance has
Fungal infections are associated with high morbidity recently published a report outlining the problem and
and mortality in the critically ill patient and lead to proposing several strategies of tackling the issue of the
very high healthcare costs. The prevalence of fungal increase in antimicrobial resistance.
13:57:49
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Table 12.5 Microorganisms showing resistance In Spain, a country with a high prevalence of

Urgent threats C. difficile multidrug resistant organisms (MDR), a recently
Carbapenem-resistant implemented ‘zero resistance’ programme recom-
Enterobacteriaceae (CRE) mends that antimicrobials against MDR should only
Serious threats Multidrug-resistant Acinetobacter spp. be administered in patients with septic shock and a
Fluconazole-resistant Candida spp. high risk of MDR based on risk factors or knowledge
Extended spectrum beta-lactamase- of local ecology.
producing Enterobacteriaceae (ESBL) The following are risk factors for carriage of
Multidrug-resistant Pseudomonas MDR.
Carbapenemase-producing
Pseudomonas 1. Hospital admission for more than 5 days in the
Methicillin-resistant S. aureus (MRSA) last 3 months.
Concerning threats Vancomycin-resistant S. aureus (VRSA) 2. Institutionalised patients (prison, healthcare,
social centre).
3. Known previous colonisation or infection with
Which are the microorganisms causing these MDR.
issues and where are they most likely to be 4. Antibiotic course of at least a week in the previous
encountered? month, especially with one or more of the
The Centre for Disease Control has published a list following:
of the current microorganism resistance threats. We (a) Third or fourth generation cephalosporins;
present the ones most likely to be encountered in a (b) Fluoroquinolones;
cardiothoracic critical care unit in Table 12.5. (c) Carbapenems.
There have been volumes written on how to best 5. End-stage renal disease or renal-replacement
tackle the emergence of these infections in the ICU. therapy.
The key message from organisations all over the world 6. Comorbid conditions associated with colonisation
is to implement antibiotic stewardship programmes or infection with MDR, such as:
and improve the education of the ‘jobbing’ intensiv-
ists in the pharmacology of antimicrobials. (a) Cystic fibrosis;
Antimicrobial stewardship is a bundle of inter- (b) Bronchiectasis;
ventions designed to optimise and measure the (c) Chronic skin ulcers.
appropriate use of antimicrobials based on pharma- Even though these risk factors were highlighted in
codynamics and pharmacokinetic data available, the context of the Spanish healthcare system, they are
local ecology and patient and unit characteristics. internationally recognisable as the situations which
A well-run stewardship programme is a two-stage should alert most clinicians to the possibility of the
process. patient being colonised by or having an infection with
Stage 1: a MDR pathogen.
(a) Identification of patients with infection; The arsenal available to combat these infections is,
(b) Empirical antibiotics according to local policy as explained earlier, getting more and more limited.
and microbiological advice; Commonly used antibiotics to treat potential MDRs
(c) Optimised dosing according are complemented by some new preparations and
to pharmacokinetics(PK)/ combinations. Table 12.6 lists some of the most com-
pharmacodynamics(PD). monly available.
Stage 2: Learning Points
(a) Review within 72 hours with laboratory • The most common approach to empirical
results and clinical progress; antibiotic treatment in severe infections
(b) Switch to narrow spectrum antibiotics (if in the critically ill is to ‘start broad and
broad spectrum antibiotics started initially); narrow down’.
(c) Stop antibiotics if the pathology is unlikely to • Consider the most likely source of sepsis when
be infection. deciding which antibiotics to start.
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Table 12.6 Most commonly available new preparations against MDRs
Antibiotic Active against No activity Remarks

Colistin (polymyxin E) Acinetobacter spp. Serratia spp. • Emergent strains of
P. aeruginosa Providencia spp. colistin-resistant KPC
Enterobacteriaceae Burkholderia cepacia • Serious nephrotoxicity and
Most other Gram-negative aerobic Gram-positive and Gram- neurotoxicity
bacilli negative aerobic cocci
Gram-positive aerobic bacilli
Anaerobes
Tigecycline MRSA P. aeruginosa Can be used for deep-seated
VRE Proteus spp. infections, note poor lung
Carbapenemase-producing Providencia spp. penetration of this antibiotic
Enterobacteriaceae
Several ESBL strains
Carbapenems Most Enterobacteriaceae Strains of Gram-positive Emerging strains of
MSSA cocci with reduced carbapenemase-producing
P. aeruginosa penicillin sensitivity microorganisms (KPO)
ESBL
Anaerobes
Glycopeptides (vancomycin, Gram-positive cocci Gram-negative bacteria
teicoplanin) Clostridium difficile
Daptomycin MDR Gram-positive cocci, Gram-negative bacteria Inactivated by alveolar
especially MRSA and VRSA surfactant –ineffective in
VRE pneumonias
MSSA right-sided endocarditis
Linezolid MRSA Gram-negative bacteria • Reversible
VRSA thrombocytopenia
VRE • Interacts with SSRIs –
Penicillin-resistant S. pneumoniae serotonin syndrome
Fosfomycin S. aureus, including MRSA Some Pseudomonas and High potential for
Enterococcus spp. including VRE E. coli strains development of resistance
ESBL-producing K. pneumoniae under prolonged therapy
and E. coli
Ceftolozane/tazobactam Indications:
• Complicated UTI
• Complicated intra-abdominal
infections
• Complicated ventilator
associated pneumonia
Tedizolid MRSA Gram-negative • Fewer side effects than
VRSA bacteria linezolid
VRE • More bactericidal activity
than linezolid
Avibactam ESBL
Carbapenemase-producing
K. pneumoniae
Plazomicin Metallo-beta-lactamase- Phase 3 clinical trials
producing strains
MRSA
Echinocandins Fluconazole-resistant Candida spp.
Aspergillus
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• The rate of discovery of new antibiotics is lower De Pascale G, Tumabarello M. Fungal infections in
than the rate of development of multidrug ICU: advances in treatment and diagnosis. Current
resistant strains in pathogens. Opinion in Critical Care. 2015; 21: 421–429.
• In the current context of drug resistant Husain S, Sole A, Alexander BA, et al. The 2015
pathogens, antibiotic stewardship is a must. International Society for Heart and Lung
Transplantation Guidelines for the management
• In certain cases, be mindful of the of fungal infections in mechanical circulatory
pharmacokinetic and pharmacodynamics support and cardiothoracic organ transplant
changes which occur due to critical illness recipients: Executive summary. Journal of Heart and
pathophysiology. Lung Transplantation. 2016; 35: 261–282.
Neinaber JJ, Kusne S, Riaz T, et al. Clinical manifestations
Further Reading and management of left ventricular assist device-
associated infections. Clinical Infectious Diseases. 2013;
Bion J, Richardson A, Hibbert P, et al. ‘Matching 57: 1438–1448.
Michigan’: a 2-year stepped interventional programme Shekar K, Roberts JA, Ghassabian S, et al. Altered
to minimise central venous catheter–blood stream antibiotic pharmacokinetics during extracorporeal
infections in intensive care units in England. British membrane oxygenation: cause for concern? Journal of
Medical Journal Quality and Safety. 2013; 22: 110–123. Antimicrobial Chemotherapy. 2013; 68: 726–727.
doi:10.1136/bmjqs-2012-001325
Tsai D, Lipman J, Roberts JA. Pharmacokinetic/
Coley CJ II, Miller MA. Ventilator-Associated Pneumonia pharmacodynamics considerations for the
in Healthcare Associated Infections. Oxford: American optimisation of antimicrobial delivery in the critically
Infectious Disease Library OUP, 2013. ill. Current Opinion in Critical Care. 2015; 21: 412–420.
MCQs
1. A 19 year old girl is admitted to the ICU following (a) Send the patient urgently to the regional cardiac
double lung transplant for cystic fibrosis. She was surgical centre and give a dose of intravenous
known to be previously colonised with multidrug flucloxacillin and gentamicin, with instruc-
resistant Pseudomonas. After initial satisfactory pro- tions to be continued for 6 weeks or until
gress, the patient develops severe pneumonia on day microbiological advice
3 postoperatively. Talking to the anaesthetist for the (b) Keep the patient in overnight, start a vasoconstric-
case, it was a difficult intubation with a small double tor to help increase the perfusion pressure to the
lumen tube and incomplete tracheobronchial toilet brain and start piperacillin/tazobactam and gen-
may have been performed. Suspecting that this is pos- tamicin intravenously
sible contamination with the patient’s previous flora, (c) Send the patient urgently to the regional cardiac
choose which antibiotic you would consider starting. surgical centre and give a dose of intravenous
(a) Tigecycline vancomycin with gentamicin and rifampicin, with
(b) Linezolid instructions to be continued for 6 weeks or until
microbiological advice
(c) Piperacillin-tazobactam ± gentamicin
(d) Intubate the patient prior to transfer and give fluids
(d) Vancomycin with ciprofloxacin to compensate for increased capillary permeability
(e) Colistin with sepsis; start a course of rifampicin
(e) Keep the patient in overnight, start a diuretic, give
2. A 57 year old male presents to the A&E department of
fluid boluses and a vasoconstrictor to maintain
a peripheral hospital with a history of 3 weeks of fever,
MAP > 65 mmHg; start vancomycin with cipro-
chills and malaise. In the last few hours, though, he is
floxacin and fluconazole
increasingly dyspnoeic and has started to cough pink,
frothy sputum. His medical history is unremarkable 3. An acceptable initial choice of antibiotics for presumed
apart from an aortic valve replacement for a stenotic ventilator associated pneumonia in a non-penicillin-
bicuspid aortic valve 3 years previously. The cardiol- allergic patient who is otherwise progressing well
ogy registrar does a ‘quick TTE’ and, despite the poor would be:
windows, detects free aortic regurgitation and a rock- (a) Meropenem
ing valve. What would you do next? (b) Piperacillin/tazobactam
13:57:49 105
.014
106
(c) Nebulised colistin (c) Flucloxacillin, rifampicin and gentamicin and an

(d) Metronidazole and piperacillin/tazobactam echinocandin for 6 weeks
(e) Levofloxacin (d) Amphotericin for 12 weeks, metronidazole and

ceftriaxone for 6 weeks
4. A 36 year old woman with a LVAD for postpartum car-
diomyopathy is referred to the parent cardiac centre (e) Linezolid and amphotericin for 12 weeks
with fever and chills. The device has been alarming 5. The risk of CLABSI is highest with:
increased power for the last 24 hours. She has a his- (a) Line insertion in an emergency
tory of frequent driveline infections with MSSA and
C. albicans. What is the choice of antibiotics if we pre- (b) Line insertion in a septic patient
sume that LVAD infection is a possible diagnosis? (c) Line insertion at a prior infected line site
(a) Echinocandin for 8–12 weeks and vancomycin and (d) Multiple line insertions in the same vein
gentamicin for at least 6 weeks
(e) Long-term catheter insertion in the radiology
(b) Rifampicin for 6 weeks and fluconazole for department
6–8 weeks
13:57:49
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107
Blood Products and Transfusion

Chapter
13 Martin Besser
Introduction To reduce the risk of transmission of infection, all

donors complete a health questionnaire prior to donation
Along with cardiothoracic operating departments,
to identify those that may be unsuitable. Any donations
cardiothoracic intensive care units are some of the
taken are then tested for a range of infections including
greatest consumers of blood products in the world; so
HIV 1 and 2, syphilis, HTLV1 and 2, hepatitis B and
for example UK cardiac surgical centres use approxi-
hepatitis C. As of April 2016, NHSBT also commenced
mately 10% of the national supply. Furthermore, use
screening for hepatitis E negative blood for transfusion
of blood products is currently on the increase due to
to some patients who are immunosuppressed due to
a combination of factors, including advancing patient
haematological malignancy or who are scheduled for or
age, increasing burden of comorbidities, expanding
have undergone solid organ or bone marrow transplan-
use of antiplatelet therapy and greater surgical com-
tation. Several initiatives are also in place to reduce the
plexity. Importantly, transfusion of blood products
risk of transmission of Variant Creutzfeldt-Jakob disease
is associated with increased morbidity and mortal-
including leukodepletion (1999) and the use of non-UK
ity thus it is imperative to employ strategies such as
methylene blue treated plasma components or com-
patient blood management (PBM) to avoid unneces-
mercial solvent/detergent fresh frozen plasma (SD FFP)
sary transfusion and conserve precious resources.
treated pooled plasma for patients born after 1995.
Blood Products
More than 2 million donations are made each year Red Blood Cells
in the UK to National Health Service Blood and It has been shown that isovolaemic haemodilution of
Transfusion (NHSBT). From these donations, approx- normal volunteers and non-anaemic patients is tol-
imately 2,000,000 units of red cells, 300,000 units of erated to a haemoglobin of 50 g/l. Studies that have
platelets, 350,000 units of FFP and 126,000 units of assessed patients who refuse blood found that the
cryoprecipitate are prepared. The current commonly degree of preoperative anaemia affected the risk of
prescribed blood products in the UK are listed in death but did not have an effect on mortality. Hebert
Table 13.1. showed in a randomised controlled trial (TRICC) that
Blood components are not blood group specific a restrictive (70 g/l) transfusion strategy was superior
due to pooling of donors in the production process. to a liberal (90 g/l) one in ICU patients. However,
This means equilibration of interindividual varia- some doubt has been cast on this in the setting of
tion from donor to donor and the dilution of hazard- cardiothoracic surgery after a recent study reported
ous antibodies such as antineutrophil antibodies. It improved outcomes with a liberal strategy. In the
is important to note that some products have traces TITRe2 trial, patients undergoing elective cardiac
of heparin and may be potentially contraindicated surgery were randomised between 90 g/l and 75 g/l as
in heparin induced thrombocytopenia. Red cells are the transfusion threshold. Ischaemic cerebral events,
considered suitable in the UK for transfusion for up myocardial infarction, infection or acute renal failure
to 35 days post donation and are stored at 4 oC ±2 oC, within 3 months of surgery were non-significantly dif-
FFP and cryoprecipitate are usable for up to 2 years ferent. This leads to transfusion rates of 92.7% versus
and are stored at −30 oC. Platelets have a shelf life of 53.4%. Strikingly, the mortality was different, 2.6%
7 days if stored at room temperature with agitation. versus 4.2%, in the two groups with a hazard ratio
14:04:16 107
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108
Table 13.1 Comparison of blood products and components currently in use in the UK

Commercial Protein Platelet Fibrinogen II V VII VIII vWF IX X
product
Blood Packed red cells Haemoglobin trace trace trace trace trace trace trace trace trace
components <40 g/l
Platelets >240 × 109/l trace trace trace trace trace trace trace trace
FFP >50 g/l nil 0.9 g/l variable variable variable >70 U variable variable variable
Cryoprecipitate nil >0.7 g/pool variable variable variable 350 U/pool variable variable variable
Methylene blue FFP >50 g/l nil 0.7 g/l variable variable variable 50 U variable variable variable
Methylene blue cryo nil 0.7 g/pool variable variable variable 350 U/pool variable variable variable
(80% of (80% of
untreated) untreated)
Blood products Fibrinogen concentrate Riastap ® Albumin nil 20 g/l
Prothrombin complex Beriplex ® 6–14 g/l nil NA 20–60** NA 10–25** NA NA 20–31*** 22–60***
Octaplex ® 1.3–4.1 g/l nil NA 20–76*** NA 18–48** NA NA 50*** 36–60***
SD FFP 45–70 g/l nil NA NA 31 NA 28 NA NA NA
* Assumed to be 100% activity but donors will vary 70–100%.

** Prior to freezing.
*** Per ml reconstituted.
Beriplex ® and Riastap ® are trademarks of CSL Behring.
Octaplex ® is a ® trademark of Octapharma.
of 1.67 (1.00–2.67) (p = 0.045) favouring the higher an interesting alternative ADP-inhibitor that allows
threshold. rapid platelet function recovery within a few hours
Accepted side effects of transfusion are infection, of stopping administration. Despite the recent devel-
immune reactions, volume overload, immune sup- opment of near patient platelet function testing,
pression, and red cell and HLA allo-immunisation. the problem remains that the platelet function test-
General recommendations agree that a Hb of <70 g/l ing becomes abnormal with reducing platelet count
is an indication for transfusion; however when the (around 75 × 109/l for the Multiplate). Moreover, the
Hb is >70 g/l the circumstances of the patient need to treatment of confirmed or assumed platelet dysfunc-
be taken into account and the risk/balance of trans- tion is platelet transfusion. The British Commission
fusion assessed. In patients with a Hb of 80–100 g/l, for Standards in Haematology have published guid-
the transfusion decision should be individualised and ance for platelet transfusion. The evidence for the
generally a transfusion is not indicated with a Hb of use of platelet transfusion is marred by the impact of
>100 g/l. However, these recommendations do not ongoing antiplatelet therapy on both the patient’s own
include patients with coronary artery disease. and transfused platelets. The general advice is to dis-
continue antiplatelet therapy where possible, taking
Platelets into account the time required to normalise platelet
We usually apply the threshold of platelets <100 × function. Platelet transfusion in patients requiring
109/
l in the immediate postoperative setting. antiplatelet therapy may increase the risk of athero-
Controversies exist for patients with concomitant sclerotic complications while not positively affecting
antiplatelet therapy. Patients exposed to antiplatelet platelet function.
therapy take several days to recover normal platelet During the intensive care stay there is contro-
function: clopidogrel (7 days), aspirin (7 days), tica- versy about the optimal platelet count for preventing
grelor (5 days) and prasugrel (7 days). Cangrelor is bleeding with a number of invasive procedures. The
14:04:16
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109
Chapter 13: Blood Products and Transfusion
XI XII XIII Protein C Protein S Antithrombin Heparin Red cell Blood White cell Clinically Donor Pathogen
stroma group contaminant important exposure inactivation or
specific subtypes reduction
trace trace trace trace trace trace No Yes Yes <5106/unit washed, 1 Leukodepletion (UK)
CMV,
negative,
irradiated
trace trace trace trace trace trace No trace Yes <5106/unit** pool, single 1 to 6 Leukodepletion (UK)
donor
apheresis,
HLA
matched
variable variable variable * variable * variable * variable * No trace** Yes <5106/unit** 1 Leukodepletion (UK)
variable variable variable variable variable variable No trace** Yes <5106/unit** 5 Leukodepletion (UK)
variable variable variable variable variable variable No trace** Yes <5106/unit** 1 Methylene blue
variable variable variable variable variable variable No trace** Yes <5106/unit** Methylene blue
No nil No No >20,000 Pasteurisation

NA NA 15–45 12–38 Yes Yes nil No No >20,000 Filtration,
pasteurisation
NA 26–62** 24–64** NA Yes nil No No >20,000 Filtration,
pasteurisation
NA NA NA 50 NA No nil Yes No >20,000 Solvent detergent
insertion or removal of epidural catheters is con- In individual patients who develop thrombocyto-
sidered safe with platelet counts >(80–100) × 109/l. penia while on ECMO, a number of possible causes
The majority of procedures, such as line insertions such as drugs, mechanical factors or immune mecha-
or chest drain removals, are safe with platelet counts nisms have to be considered. Where there is an associ-
over 50 × 109/l provided concomitant anticoagula- ated bleeding pattern this is important and the need
tion has been corrected or stopped. Our practice, for ongoing anticoagulation needs to be reviewed.
with the exception of epidurals and lumbar punc- Where reduced anticoagulation therapy can be com-
tures, is to transfuse platelets for counts <50 × 109/l pensated with measures such as increasing the flow of
prior to intervention and to not transfuse platelets the ECMO circuit, this is likely to be more effective
for counts of >80 × 109/l. Between 50 and 8 0 × 109/l than a small increment in platelet count. Any trans-
we will reserve a unit of platelets for 8 hours for the fused platelets will be subjected to the same causes of
patient in case of excessive bleeding or if the clini- thrombocytopenia as the patient, and particularly in
cian requests these. moderate thrombocytopenia are unlikely to have a
In patients on ECMO the agreed platelet threshold prolonged effect.
is currently debated. We accept 100 × 109/l in a bleed- We assume that a unit of platelets will contain a
ing patient but have had individual patients where we minimum of 250 × 109/l per adult therapeutic dose.
tried to achieve higher platelet counts due to concom- In a healthy adult we assume a daily platelet produc-
itant intracranial bleeding with a continued need for tion of 10 × 109/l. A platelet transfusion is clinically
heparin anticoagulation. Others advocate thresholds most effective in a patient with thrombocytopenia.
as low as 20 × 109/l. The coagulation system in adults The platelet recovery following a fixed dose infu-
and children is fundamentally different and therefore sion of platelets is highly variable and is dependent
it is not likely that the same threshold can be applied on the original reason for thrombocytopenia in the
for both groups of patients. patient. It is bound to be optimal in a patient with
14:04:16 109
.015
110
lack of production but far less satisfactory in a patient Ranucci et al. recently reported a prospective,
with platelet destruction. There are a number of spe- randomised, blind study of 116 patients under-
cific cardiothoracic interventions that will reduce the going high risk cardiac surgery with an expected
platelet recovery in a given patient such as extracor- cardiopulmonary bypass duration of >90 minutes.
poreal membrane oxygenation (ECMO) and intra- Patients received fibrinogen concentrates after pro-
aortic balloon pump (IABP). tamine administration and prothrombin complex
Human platelet concentrates express very few concentrates (PCCs) if bleeding persisted. Patients
AB antigens and are suspended in less than 50 ml receiving fibrinogen had a significantly lower rate of
of plasma. For this reason ABO groups can be over- any allogeneic blood product transfusions, includ-
ridden in case of an emergency. Platelets do how- ing PRBCs and FFP. Postoperative bleeding was also
ever express HLA class I antigens, which can lead to reduced in the fibrinogen treated patients (median,
antibody formation causing platelet refractoriness 300 ml; interquartile range, 200 to 400 ml) com-
(defined as repeated platelet increments of <5 × 109/l). pared with the control patients (median, 355 ml;
Red cells are more potent HLA type sensitisers than interquartile range, 250 to 600 ml). However, the
platelet transfusions and multiparous women are par- recently published REPLACE-trial comparing the
ticularly at risk. The UK national blood service is able early aggressive use of fibrinogen concentrate in
to provide HLA class I typing and antibody screening patients undergoing aortic surgery with placebo, on
with a view to providing HLA selected/matched plate- the background of a defined transfusion algorithm
lets. These products are considerably more expensive with platelets and FFP, did not demonstrate clinical
than standard platelets but may lead to better incre- benefit.
ment and thus overall reduction in platelet usage. All
HLA matched platelets must be irradiated. Fresh Frozen Plasma and Prothrombin
Complex Concentrate
Cryoprecipitate and Fibrinogen Concentrate Fresh frozen plasma may increase clotting factor
Fibrinogen is a critical haemostatic factor for the activity by up to 30% with administration of 15 ml/
development of effective local clotting in all surgi- kg. The absolute increment depends on the baseline
cal patients, and in particular for the management factor activity in 40 ml/kg of patient plasma and may
of perioperative bleeding in cardiac surgical patients. be considerably smaller if the clotting factor levels are
Normal fibrinogen levels are 200–400 mg/dl in the nearly normal. There may be considerable variation in
non-parturient, but may be >400 mg/dl during the the concentration of individual factors such as factor
third trimester of pregnancy. The optimal transfusion XI or IX between donors. In some congenital coagu-
threshold for fibrinogen replacement is unknown. lation factor deficiencies, it may therefore be advis-
There is no RCT evidence for the transfusion thresh- able to use pooled products to minimise these effects
old of 1 g/dl but it has been accepted in clinical prac- between donors.
tice. More recently, higher thresholds for fibrinogen Prothrombin complex is a pooled plasma prod-
replacement have been advocated with thresholds of uct that contains factors II, VII, IX and X as well as
up to 2 g/dl. The massive transfusion guidelines pub- Protein C and S. It is licensed for use in acquired defi-
lished by the BCSH advise use of a cut-off of 1.5 g/dl as ciency of the vitamin K dependent clotting factors.
the threshold, as do the NICE transfusion guidelines The most recent guidelines (2015) on the treatment of
of November 2015. massive haemorrhage explicitly advise against the use
An adult dose of cryoprecipitate (10 units or 2 of prothrombin complex in massive transfusion out-
pools) is equivalent to 2–4 g of fibrinogen concentrate. side studies. The main advantage of using PCC over
Based on the relative content of fibrinogen per ml, FFP is the reduced volume and easier administration.
fibrinogen concentrate should be superior to cryopre- An FFP equivalent dose is 15 U/kg, and there are pub-
cipitate in restoring low fibrinogen levels. However, lished dosing recommendations for warfarin reversal
cryoprecipitate also contains factors such as vWF based on baseline INR with up to 50 U/kg. The avail-
and factor XIII which may be of therapeutic benefit. able PCCs also contain traces of heparin so are con-
Importantly, a therapeutic dose of 4 g of fibrinogen is traindicated for the reversal of warfarin in patients
four times as expensive as cryoprecipitate. with HIT.
14:04:16
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111
Recombinant Activated Factor VIIa Platelets may also have been exposed to antiplatelet
agents in the immediate preoperative phase, which
Recombinant FVIIa is used off- label as a prohae-
will have reduced platelet activation further. High
mostatic agent for life threatening hemorrhage.
doses of unfractionated heparin inhibit the majority
Its mechanism of action is thought to be related to
of the serin proteases in an antithrombin dependent
binding with tissue factor (TF) expressed at the site
manner. If administered in high doses, the half-life of
of vascular injury to locally produce thrombin and
heparin is prolonged, ranging between 30 and 90 min-
amplify haemostatic activation. Controlled clinical
utes. Elimination is via renal and hepatic mechanisms
trials report the incidence of thrombotic complica-
in addition to poorly delineated pathways involving
tions among patients who received rFVIIa to be rela-
the macrophages and endothelial cells. Sequestration
tively low and similar to that among patients who
sites can be a source of heparin rebound, which is
received placebo. In the most recent cardiac surgi-
sometimes observed in patients who have received
cal study, patients bleeding postoperatively >200 ml/
exceedingly high doses of heparin during CPB for
hour were randomised to placebo, 40 µg/kg rFVIIa or
up to 12 hours. Tissue debris is aspirated by cardi-
80 µg/kg rFVIIa. Primary endpoints were the number
otomy suckers from the surgical field and mixed with
of patients suffering critical serious adverse events.
the other blood and recirculated, adding a source of
Secondary endpoints included rates of reoperation,
extrinsic clotting factor activation.
blood loss and transfusions. Although more adverse
events occurred in the rFVIIa groups, they did not
reach statistical significance. However, after ran-
Diagnostic Testing
domisation, significantly fewer patients in the rFVIIa The majority of cardiac patients have postoperative
group underwent a reoperation because of bleeding or thrombocytopenia and the clotting factors, if meas-
needed allogeneic transfusions. ured, can be as low as 25–50% of baseline immediately
after separating from CPB. A gradual recovery occurs
over the next 2–4 days. No single laboratory test has
Bleeding and Coagulopathy been shown to be predictive of postoperative clinical
About 50% of cardiac surgical patients receive red bleeding and unselected correction of platelet count
cells, 30% of which also receive blood product com- or fibrinogen has had only disappointing results.
binations including platelets or plasma. Established
risk factors for transfusion include preoperative Preoperative Screening
anaemia, low body mass index, complexity and It is currently accepted practice to screen aPTT and
urgency of surgery. PT preoperatively along with full blood count (FBC).
The cell based model of haemostasis is complex The reason for screening PT and aPTT is an anachro-
and not easily reproducible in vitro (Figure 13.1). nism dating back to when warfarin and unfraction-
Haemostasis is initiated following tethering of plate- ated heparin were the main anticoagulants in use.
lets to a site of vascular injury through vWF and The FBC is more important than ever in that it allows
GPIb/V/IX. The platelet membrane undergoes activa- screening for preoperative anaemia or thrombocyto-
tion and mediators are released. Traces of tissue factor penia, which may be amenable to preoperative inter-
stabilise the factor VIIa, which in turn activates traces vention. Generally we accept platelet counts >90 ×
of IXa, Xa and thrombin. This sets off an autofeed- 109/l, aPTT <38 s and PT <18 s, assuming the patient
back mechanism that propagates self-activation and is not on anticoagulants. A bleeding score is more use-
results in fibrin polymerisation, followed by thrombin ful to identify patients with a potential undiagnosed
inactivation. bleeding disorder.
The effects of CPB on haemostasis are also com-
plex and multifactorial. During surgery the major- Blood Tests Used To Assess and Direct Treatment of Post
ity of the surgical field is bypassed by the circulating CPB Coagulopathy
blood; the patient’s blood is haemodiluted with crys- The majority of centres now use a combination of lab-
talloid and albumin. Hypothermia in combination oratory and point-of-care assays in combination with
with partial activation of the clotting cascade prolongs clinical assessment to guide transfusion of products
the clotting reaction further. Primary haemostasis is according to predefined algorithms (see Figure 13.2);
impaired by platelet consumption and degranulation. for further details see Chapter 36.
14:04:16 111
.015
112
HK
FXII
PK
FXIIf
FXIIa
K
FXI PL, FVIIIa, Ca

HK
intrinsic
PL, HK, Zn, Ca FXIa
extrinsic FIXa
FIX
PL, FVIIIa, Ca FXIII
.015
FVII FVIIa FXa FIIa
PL, TF, Ca FX FII FXIIIa

FI
14:04:16
Leucocyte
Fibrin Cross-linked Fibrin
tPA
PAF
RESTING
ADP
Complement
PG, TXA2, NO, 5HT, OR,
lysosome, IL-1, Histamine, NET
Endothelial Cell
FRAGMENTED NEWLY
ACTIVATED
FORMED
Figure 13.1 Cell based model of haemostasis. Contact activation occurs with activation of the four contact factors: K, PK, HK and XII. This leads to activation of the intrinsic pathway and activated
complement. Both the activation of the complement pathways and the formation of thrombin activate platelets and lead to platelet aggregation and fragmentation. Platelet activation, in turn,
activates endothelial cells and causes release of tPA platelet activation.
K kallikrein, PK prekallikrein, HK high-molecular-kininogen, F factor, a activated form, f fragmented form, PG prostaglandin, NO nitrous oxide, TXA2 thromboxane A2, OR oxygen radicals, 5HT
serotonin, IL1 interleukin 1, PAF platelet activating factor, tPA tissue plasminogen activator. (A black and white version of this figure will appear in some formats. For the colour version, please refer to
the plate section.)
113
Admission to ICU
yes
Blood loss
no No therapy
> 3ml/kg/hr
no
50 mg of protamine yes ACT >110% of

baseline
no
2 pools of
cryoprecipitate Fibrinogen
yes
or 4 g fibrinogen <1.5 g/l
concentrate
no
Reassess patient 1 unit of platelets yes Platelets <100 ×

109/l
no
15 ml/kg of FFP yes Pt >25 s
no
aPTT >48 s
TT<25 s
no
aPTT >48 s
50 mg protamine yes
TT>25 s
no
Consider
tranexamic acid or
15U/kg of
DD AVP Patient on
prothrombin yes warfarin preop
complex
no
Figure 13.2 Part of the rationale for use of blood products is the use of preagreed transfusion algorithms to restore near normal haemostasis.
Laboratory Based Tests essential. Generally it is assumed that thrombocyto-

The conventional laboratory tests in use are the penia will respond clinically to platelet transfusions
PT/INR, aPTT, Clauss fibrinogen and throm- up to 100 ×109/l. PT >20 s and aPTT >48 s correct with
bin time. Others include anti-Xa level. FBC is also FFP. These screening tests tend to become prolonged
14:04:16 113
.015
114
when the levels of some individual factors have

decreased to 40% or less.
Blood Conservation
PBM is an international initiative based on the
The main drawback of using laboratory based
Australian experience of using a multimodal approach
assays is the slower turnaround time, which may be as
to optimise red cell mass, minimise blood loss and
long as 40 minutes. Furthermore, these assays are sen-
harness the physiological tolerance of anaemia, so as
sitive to high heparin levels. Thrombin time allows the
to reduce the need for transfusion, improve patient
detection of heparin and interpretation of prolonged
outcomes and ensure that blood products are available
clotting tests in complex patients. It is more sensitive
for those patients that absolutely require transfusion.
to heparin than aPTT, and a TT value >25 s suggests
The UK Department of Health has published guide-
heparin contamination. In the context of recently dis-
lines which can be downloaded freely and encompass
continued warfarin therapy, mildly prolonged aPTT
a range of interventions beginning with rapid diagno-
and PT may hint at potentially correctable deficits in a
sis of preoperative anaemia and correction of revers-
patient with protracted bleeding. Dabigatran or arga-
ible causes when possible prior to surgery, the use of
troban may similarly potentially produce falsely low
cell salvage and adjuncts such as fibrin glue, along with
fibrinogen results.
targeted reversal of anticoagulants and algorithms to
Point-of-Care (POC) Testing correct coagulopathy, so as to minimise perioperative
blood loss, and use of a restrictive policy of diagnostic
POC testing is firmly establishing itself in the set-
testing to reduce the impact of repeated blood sam-
ting of cardiothoracic surgery. The benefit of these
pling on postoperative haemoglobin.
tests is the rapid turnaround and the ability to detect
hypofibrinogenaemia at the POC. The drawback is
the relative insensitivity to some of the more subtle Future Outlook: Anticoagulant
imbalances of coagulation such as warfarin or heparin Reversal with Beriplex, Idaricuzimab
therapy for which laboratory based assays have been
validated and have a long track record.
and Adexanet Alfa
The two dominant technologies are thrombo Four new oral anticoagulants have come on the market
elastography (TEG) and rotational thromboelasto over the past 5 years. While the adoption was slow ini-
metry (ROTEM). A third, the Sonoclot, was evaluated tially, now patients present for urgent or elective surgery
by NICE in 2014 but was not deemed suitable to be while on these drugs. There are set recommendations
used outside a clinical trial. All the viscoelastic assays by the manufacturers with regard to pausing treatment
benefit from a number of activator kits which usu- prior to surgery based on renal function and risk of sur-
ally include a PTT like reagent with kaolin or celite, gery. Tranexamic acid and correcting other correctable
a tissue factor based activator (EXTEM or fastTEG), factors like thrombocytopenia may also help.
a fibrinogen activator (functional fibrinogen, or Prothrombin complex has become the reversal
FIBTEM) and a heparinase containing Celite or kaolin agent of choice of the novel anticoagulants with doses
assay. Manufacturers are developing a cartridge based of 25–50 IU/kg (albeit not licensed). This has now
solution that allows the simultaneous assessment of been superseded for dabigatran by idaricuzimab, a
several of the assays at once in varying combinations monoclonal antibody for dabigatran. We are expect-
to improve reliability. ing that adexanet alfa (a dummy factor Xa molecule)
The TEG is able to assess platelet function in will receive a license in the near future for Xa inhibi-
addition to the above tests by making the reaction tors for specific reversal.
dependent on ADP platelet activation or arachidonic
acid based activation. Another potentially useful test Learning Points
is the Multiplate platelet function assay. This utilises • Blood products and components vary in their
electric impedance to detect platelet function/aggre- indications, and internationally and randomised
gation in whole blood. Results are available in under control trials to determine their optimal use are
10 minutes but one of the problems with the test is the lacking.
interference from low platelet counts, which may be a • Recombinant products are only available for a
secondary reason for a lack of detectable platelet func- minority of indications such as congenital factor
tion perioperatively. VIII deficiency.
14:04:16
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115
• Recombinant factor VIIa was inferior to best

conventional management in cardiothoracic
Further Reading
http://www.b-s-h.org.uk/guidelines/guidelines/
surgery. use-of-platelet-transfusions/
• Point-of-care testing has advantages over
www.nice.org.uk/guidance/ng24
laboratory testing of turnaround time and global
nature. Laboratory assays by comparison have a http://transfusion.com.au/transfusion_practice/
blood_conservation
defined advantage in their reproducibility and use
in transfusion algorithms. Weiskopf RB, Viele MK, Feiner J, et al. Human
cardiovascular and metabolic response to acute, severe
• Prothrombin complex has become the
isovolemic anemia. Journal of the American Medical
unlicensed reversal agent of choice for direct oral Association. 1998; 279(3): 217–221.
anticoagulants (DOACs). Specific reversal agents
will probably be available in the near future.
MCQs
Which of the following statements is true? (d) There is no role for the aPTT and PT in postopera-
1. UK Plasma: tive quantification of coagulopathy
(a) Is being used to manufacture plasma derived sin- (e) DOAC should be reversed with activated pro-
gle factor concentrates where so far there is no thrombin concentrate
recombinant option 4. Blood products:
(b) Is no longer used (a) Red cells can be stored for up to 2 years
(c) Is used in patients born after 1.1.1996 only if (b) FAC sorted platelets can be ordered by the
treated with methylene blue NHSBT
(d) Is now only used for FFP, cryoprecipitate and (c) Platelets express class I HLA antigens
platelets
(d) Red cell transfused patients will not develop HLA
(e) Is pooled before use class I antibodies
2. Point-of-care testing: (e) Platelet increments should be performed 7 days
(a) Has been endorsed by NICE after cardiothoracic after administration
surgery 5. Transfusion associated risks:
(b) Is advocated for warfarin reversal (a) Greatest risk to the patient is viral transmission
(c) Leads to more restrictive cryoprecipitate or (b) Patients who refuse blood on grounds of lack of
fibrinogen use safety of the blood supply should be offered con-
(d) Increases the use of FFP comitant antiretrovirals
(e) Should not be performed intraoperatively (c) Patients who refuse blood should be offered autolo-
gous predeposit of blood
3. Laboratory based testing:
(d) Prothrombin complex is a recombinant product
(a) The thrombin time is sensitive to heparin overhang
(e) A liberal transfusion threshold >90 g/l was superior
(b) The anti-Xa levels may be falsely low in HIT to 75 g/l in the T2 study
(c) Clauss fibrinogen is unaffected by thombin inhibi-
tors such as dabigatran
14:04:16 115
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116
Fluid Administration
Chapter
14 Vasileios Zochios and Kamen Valchanov
Introduction intracellular (potassium) and extracellular (sodium)

ions. In addition, proteins and large molecules main-
Intravenous fluid administration is performed in crit-
tain the colloid distributions between intracellular,
ically ill patients to maintain fluid volume homeosta-
interstitial and intravascular spaces.
sis and to achieve many other goals. Intensivists and
The fate of any intravenous fluid given into the
perioperative physicians who care for the cardiotho-
vascular compartment depends on many factors
racic critically ill patient must appreciate that fluids
including the electrolyte and colloid (if any) compo-
are ‘drugs’ and therefore it is necesssary to understand
sitions, the patient’s intravascular volume status, the
their physiology and pharmacology. Appropriate fluid
total volume of fluid administered, and the integrity
resuscitation is often the first intervention for the
of endothelial glycocalyx. The endothelial glycoca-
haemodynamically unstable patient. There is ongoing
lyx modulates vascular permeability and inflamma-
debate regarding whether the fluid chosen for these
tion and according to the Starling model it is a key
patients should be a crystalloid solution (i.e. isotonic
determinant of fluid disposition. The primary forces
saline, Ringer’s lactate) or a colloid containing solu-
defining transcapillary fluid movement and the coun-
tion (i.e. albumin solution, hyperoncotic starch).
terbalancing process of fluid movement into the vas-
Large international surveys have shown that choice
cular space in a normal and damaged vasculature are
of fluid is mostly a matter of institutional preference
shown in Figure 14.1. It has been shown that CPB is
rather than due to specific procedural/patient related
associated with loss of glycocalyx integrity and micro-
factors.
vascular dysfunction. Interestingly, significant shed-
ding of the glycocalyx also occurs during off-CPB
Pathophysiology procedures. In critical illness, including post-CPB/
There are several determinants in assessing the need postoperative states, endothelial glycocalyx denuda-
for intravascular volume replacement in the context of tion causes high transcapillary movement of fluid
cardiac surgery: (i) blood loss, (ii) increasing vascular leading to tissue oedema and inadequate intravas-
capacitance as often occurs with patient rewarming, cular volume expansion after intravenous fluids are
(iii) third space fluid losses secondary to cardiopul- administered.
monary bypass (CPB) induced systemic inflamma-
tion, and (iv) increased cardiac preload requirements
in the setting of transient cardiac ischaemia –reper- Fluids in the Cardiothoracic ICU
fusion injury, myocardial stunning and reduced ven-
tricular compliance. Colloids Versus Crystalloids
Total body water for the average 70 kg adult male is There is a lack of prospective data with special regard
about 45 l of which 30 l (65%) is intracellular and 15 l to ‘ideal’ fluid in the cardiac surgical patient popula-
(35%) is extracellular fluid. The extracellular space can tion. Colloid fluids would be expected to produce a
be subdivided into interstitial space (10l) and intravas- much larger volume expanding effect. Usual teaching
cular space (5 l). All three compartments also contain suggests that the colloid to crystalloid volume expan-
electrolytes, including ions and larger molecules. The sion efficacy is 1:3 (300% greater efficacy for colloids),
cellular membranes maintain potential differences whereas the colloid to crystalloid ratio for volume
via a complex differential concentration between expansion in adequately powered and well-designed
14:08:11
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117
Chapter 14: Fluid Administration
Normal Vasculature Damaged Vasculature
Vascular Endothelium Vascular Endothelium
Glycocalyx Glycocalyx
πc Pc Capillary Flow πc Pc
Capillary lumen Capillary lumen
σ Kf σ Kf less glycocalyx
less tight
junctions
Interstitium Interstitium
πi Pi πi Pi
Jt Lymphatic Flow more oedema

formation
Figure 14.1 The opposing forces defining the steady state net flow of fluid from the capillary into the interstitial space are defined by the
hydrostatic pressure differences between the capillary lumen pressure (Pc) and interstitial pressure (Pi) as opposed by the filtration coefficient
(Kf) which itself is a function of the vascular endothelial cell integrity and the intraluminal glycocalyx. This net efflux of fluid out of the
capillary into the interstitium is blunted by an opposing oncotic pressure gradient moving fluid in the opposite direction because capillary
oncotic pressure (πc) is greater than interstitial oncotic pressure (πi). And like hydrostatic pressure dependent flow, oncotic dependent flow
is blunted by the reflection coefficient (σ), which like Kf is a function of the glycocalyx and vascular endothelial integrity. Under normal
conditions (left side), both Kf and σ are high, minimising fluid flux resulting in a slight loss of plasma into the interstitium which is removed by
lymphatic flow. However, if the vascular endothelium and glycocalyx are damaged (right side), oncotic pressure gradients play a minimal role
because a large amount of protein-rich plasma translocates into the interstitial space, minimising the oncotic pressure gradient, whereas the
constant Pc promotes massive fluid loss and interstitial oedema.
Adapted from Lira and Pinsky (2014), permission to reproduce granted under SpringerOpen general terms.
randomised controlled trials (RCTs) was 1:1.2–1:1.4 hypernatraemia, hyperchloraemia and acidosis. There
(approximately 30% greater efficacy for colloids). The was a black box warning from FDA for heat starch.
contents of solutes in colloid and crystalloid solutions In a 9 y ear multicentre open label trial (CRISTAL),
are presented in Tables 14.1 and 14.2. 2857 patients with hypovolaemic shock, due to any
It would stand to reason that early during elec- cause, were randomly assigned to fluid resuscitation
tive cardiac surgery colloid fluids may have a better with colloid or crystalloid. There was no difference
volume expansion effect than crystalloids as capillary in 28 day mortality or need for RRT between the two
pressures are likely to be normal and loading with arms. Patients treated with colloids had more mechan-
crystalloids would produce a dilutional effect on ical ventilation free days (13.5 versus 14.6 days) and
plasma oncotic pressure leading to tissue oedema and vasopressor therapy (15.2 versus 16.2 days), as well as a
a reduced volume expansion effect. lower 90 day mortality (31% versus 34%). However, the
Crystalloids are preferred over colloid contain- open label design and heterogeneity of fluids that were
ing solutions for the management of patients with compared between the groups limit confidence in the
severe hypovolaemia not due to bleeding. Saline solu- apparent benefit of colloid solutions in this population.
tions seem to be as effective as other crystalloid solu-
tions and colloid containing solutions, and are much Albumin
less expensive. It is recommended that hyperoncotic In theory, albumin has two possible advantages over
starch solutions are avoided as they increase the risk crystalloid solutions: (i) more rapid plasma volume
of acute kidney injury, need for renal replacement expansion, since the colloid solution remains intravas-
therapy (RRT) and mortality. They may also lead to cularly (in contrast to saline, three quarters of which
14:08:11 117
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118
Table 14.1 Composition of currently available crystalloid solutions
Fluid/solute Na+ K+ Cl− Ca2+ Mg2+ Osmolarity Lactate Gluconate Acetate Glucose
mEq/l mEq/l mEq/l mEq/l mEq/l mOsm/l mEq/l mEq/l mEq/l g/l
Plasma 142 4 103 5 3 290 2 — — 1
NaCl 0.9% 154 — 154 — — 230 — — — 50
.016
Dextrose 5%
NaCl 0.45% 77 — 77 — — 203 — — — 50
Dextrose 5%
14:08:11
NaCl 0.9% 154 — 154 — — 308 — — — —
Lactated Ringer’s 130 4 109 3 — 273 28 — — —
Dextrose 5% — — — — — 252 — — — 50
Plasmalyte 148 140 5 98 — 3 294 — 23 27 —
Normasol 140 5 98 — 3 294 — 23 27 —
119
Table 14.2 Composition of currently available colloid solutions
Fluid/solute Osmolarity pH Na+ K+ Ca2+ Cl−

mOsm/l mEq/l mEq/l mEq/l mEq/l
Gelofusine 274 7.4 154 <0.4 <0.4 125
Hetastarch 308 4.0–5.5 154 — — 154
Haemaccel 301 7.4 145 5 6.25 145
Pentastarch 326 5.0 154 — — 154
Albumin 4.5% 7.4 <160 <2 — 136
enters the interstitium) and (ii) lesser risk of pulmo- anything but ‘normal’ or ‘physiological’ as it is slightly
nary oedema, since dilutional hypoalbuminaemia will hypertonic and contains equal amounts of sodium and
not occur. Well-designed RCTs and meta-analyses have chloride making it hypernatraemic and very hyper-
failed to demonstrate benefits from the use of albumin. chloraemic relative to plasma. Administration of high
However, in some cardiothoracic intensive care units volume ‘normal’ saline will result in hypernatraemia,
albumin remains the colloid of choice for patients hyperchloraemic acidaemia leading to renal vasocon-
undergoing lung transplantation and pulmonary striction and reduction in renal blood flow. This has
endarterectomy when volume expansion is needed in led to suggestions that physiologically buffered fluids
the immediate postoperative period, in an attempt to with a chemical composition that approximates extra-
reduce the risk of early reperfusion lung injury. cellular fluid (e.g. Ringer’s lactate solution, Hartman’s
solution, Plasma-lyte 148, Accusol) are used instead
Hydroxyethyl Starch (HES) of ‘isotonic’ saline for large volume resuscitation.
A recent RCT which enrolled healthy volunteers, and
Use of hyperoncotic starch solutions has been associ-
large observational series, have demonstrated that
ated with increased incidence of acute kidney injury
adverse effects associated with saline use were not evi-
(AKI) and high mortality in some studies. In a RCT,
dent when physiologically buffered fluids were used.
7000 patients were randomised to receive 6% HES
or normal saline for all fluid resuscitation until ICU
discharge. There was an increased incidence of AKI Hypertonic Solutions
requiring RRT in the HES group compared with the Hypertonic solutions typically used in cardiac sur-
saline group (5% versus 5.8%). Two meta-analyses, gery include 2–7% saline. They have been used in
one of which excluded seven trials that were retracted an attempt to minimise volume overload and prod-
due to scientific misconduct of one investigator, found uce cellular dehydration in the context of cerebral
that compared to conventional fluid resuscitation reg- oedema. The majority of the trials of hypertonic
imens, HES was associated with increased risk of mor- solutions have been in patients with traumatic brain
tality and need for RRT. HES associated AKI appears injury. The results cannot be extrapolated for the gen-
to be related to pinocytosis of metabolites into renal eral cardiac surgical population. However, cardiac
proximal tubular cells after glomerular filtration. HES surgical patients with cerebral oedema may bene-
has also been associated with increased risk of bleed- fit from hypertonic saline solutions on an individual
ing, which is probably due to impaired fibrin polymer- basis. Studies examining use of hypertonic solutions
isation and decreased factor VIII, vWF and XIII levels did not examine their effect on renal function and
and not associated with haemodilution. Given the fact reported a high incidence of hypernatraemia.
that the cardiac surgical patient population is at risk of
AKI and coagulopathy anyway, the use of HES in the Fluid Balance Management
setting of cardiac surgery is not recommended. Positive fluid balance has been associated with worse
outcomes in some but not all critically ill patient pop-
Crystalloids ulations. A recent observational study that included
One of the most commonly used crystalloid solutions a large cohort of medical, surgical and cardiothoracic
is 0.9% sodium chloride or ‘normal’ saline, which is ICU patients showed that positive fluid balance at the
14:08:11 119
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120
time of ICU discharge was associated with increased result in impaired gas exchange, need for prolonged
risk of death, after adjusting for markers of illness mechanical ventilation, prolonged length of stay and
severity and chronic medical conditions, particularly high mortality.
in patients with underlying heart or kidney disease.
A secondary analysis of the FACTT trial demon-
strated that patients with ARDS who developed AKI Fluid Responsiveness
had a higher mortality (independent of a conservative In the cardiothoracic intensive care populations,
or liberal fluid administration strategy). This study reduced cardiac output is treated by correcting the
demonstrated some evidence of causality, as diuretic main determinants: heart rate, myocardial contractil-
use was associated with a protective effect, potentially ity, afterload and preload. When preload is reduced
due to its effect on fluid balance. When the diuretic and fluid replacement is needed then the strategy is
effect was adjusted for fluid balance, the protective usually to administer the minimum fluid required to
effect was attenuated, thus potentially suggesting that achieve optimising of cardiac output for the particu-
the modulation of fluid balance promoted the benefit. lar moment of time. Overenthusiastic fluid adminis-
Intravenous fluid administration is a common tration in the cardiac surgical population can lead to
intervention used for both the prevention and treat- increased preload (which is more difficult to treat),
ment of AKI. The pathogenesis of AKI in cardiac surgi- overstretching of myocardial fibres, pulmonary
cal patients is multifactorial, not only due to perturbed oedema and generalised oedema. However, on occa-
haemodynamics but also the result of direct cellular sions fluid administration in cardiothoracic criti-
injury as well as indirect injury from inflammation cally ill patients is required. In general this is guided
and microcirculatory changes. AKI with oliguria as by imaging of the heart and IVC or cardiac output
well as fluid resuscitation often results in accumula- monitors. Sometimes, a more pragmatic way of moni-
tion of excess total body fluid. This fluid accumulates toring fluid administration can be measuring fluid
in all tissues of the body, and through the interstitial responsiveness.
space, as well as remaining within the vascular space, The definition of fluid responsiveness varies
resulting in increased venous pressure. The presence according to the clinical or research setting. A recently
of oliguria is associated with a poor prognosis; how- proposed definition is ‘an increase in a physiologic
ever, it remains unclear whether this is due to severity parameter, preferably cardiac output, within 15 min-
of injury or due to fluid overload. Most studies to date utes superseding twice the error of the measuring
have been conducted in the general ICU population. technique after a 15-minute administration of 6 ml
Similar findings have been reproduced in the cardiac kg–1 of crystalloids’. In the critical care setting, only
surgery population, as early administration of fluid 50% of haemodynamically unstable patients are ‘fluid-
can lead to AKI. In a prospective observational cohort responders’ when the fluid bolus is given on ‘clinical
of 100 patients undergoing cardiac surgery, those grounds’. This emphasises that fluid loading is not
patients in the quartile receiving the highest volume always the correct therapy for a clinically hypoper-
of fluid suffered the highest degree of AKI. This study fused patient and that ‘non-responders’ are exposed
was limited by the small number of patients included. to the risks of volume overload, systemic and pulmo-
It has been demonstrated that positive fluid bal- nary oedema and tissue hypoxia. In other words, fluid
ance in the first 3 postoperative days is associated with responsiveness is a measure of ‘preload dependence’
primary graft dysfunction after lung transplantation. or ‘preload reserve’ but not all ‘fluid-responders’ nec-
Patients undergoing pulmonary endarterectomy con- essarily need volume loading.
stitute a unique patient population at risk of develop- Examples of clinical measures include static and
ment of ARDS due to high permeability lung injury. dynamic parameters. The static parameters (such as
Therefore restrictive fluid management strategies and central venous pressure) are described as having little
adequate diuresis in the first 48 hours (aiming for 2 l value; however, the dynamic parameters (stroke vol-
negative fluid balance) is of paramount importance. ume variation and pulse pressure variation, as meas-
Negative fluid balance should also be maintained dur- ured using a number of monitors) are shown to be
ing the first week after lung resection surgery. Fluids good physiological determinants of fluid responsive-
should be limited because lung resection decreases ness. Passive leg raise is an increasingly popular fluid
the pulmonary vascular bed and overhydration will responsiveness assessment tool. In patients receiving
14:08:11
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mechanical circulatory support (extracorporeal life perfusion in healthy volunteers. Annals of Surgery.
support, ventricular assist devices, intra-aortic bal- 2012; 256: 18–24.
loon pump), transthoracic and transoesophageal Finfer S, Bellomo R, Boyce N, et al. A comparison of
echocardiography are invaluable diagnostic tools albumin and saline for fluid resuscitation in the
that can be utilised to assess fluid responsiveness and intensive care unit. New England Journal of Medicine.
intravascular volume status. 2004; 350: 2247–2256.
Fulop T, Pathak MB, Schmidt DW, et al. Volume-
Learning Points related weight gain and subsequent mortality in
acute renal failure patients treated with continuous
• Fluids are drugs. renal replacement therapy. ASAIO Journal. 2010;
• The integrity of the endothelial glycocalyx 56: 333–337.
appears to have a major role in fluid exchange and Gheorghe C, Dadu R, Blot C, et al. Hyperchloremic
distribution. metabolic acidosis following resuscitation of shock.
• Starch solutions should be avoided during and Chest. 2010; 138: 1521.
after cardiothoracic surgery. Hahn RG. Volume kinetics for infusion fluids.
• Physiologically buffered fluids have some Anesthesiology. 2010; 113: 470–481.
advantages including maintenance of renal Lee J, de Louw E, Niemi M, et al. Association between fluid
perfusion and avoidance of acid-base balance and survival in critically ill patients. Journal of
Internal Medicine. 2015; 277: 468–477.
imbalance.
• Bedside assessment of fluid responsiveness should Lira A, Pinsky MR. Choices in fluid type and volume
during resuscitation: impact on patient outcomes.
always precede fluid loading.
Annals of Intensive Care. 2014; 4: 38.
Further Reading Marik PE, Baram M, Vahid B. Does central venous pressure
predict fluid responsiveness? A systematic review of
Annane D, Siami S, Jaber S, et al. Effects of fluid the literature and the tale of seven mares. Chest. 2008;
resuscitation with colloids vs crystalloids on 134: 172–178.
mortality in critically ill patients presenting with
Michard F, Teboul JL. Predicting fluid responsiveness in
hypovolemic shock: the CRISTAL randomized trial.
ICU patients: a critical analysis of the evidence. Chest.
Journal of the American Medical Association. 2013;
2002; 121: 2000–2008.
310: 1809.
Morgan TJ. The meaning of acid-base abnormalities
Banks DA, Pretorius GV, Kerr KM, et al. Pulmonary
in the intensive care unit: part III –effects of fluid
endarterectomy: part I. Pathophysiology, clinical
administration. Critical Care. 2005; 9: 204.
manifestations, and diagnostic evaluation of chronic
thromboembolic pulmonary hypertension. Seminars Myburgh JA. Fluid resuscitation in acute medicine: what
in Cardiothoracic and Vascular Anesthesia. 2014; is the current situation? Journal of Internal Medicine.
18: 319–330. 2015; 277: 58–68.
Bouchard J, Soroko SB, Chertow GM, et al. Fluid Myburgh J, Cooper D, Finfer S, et al. Saline or albumin
accumulation, survival and recovery of kidney for fluid resuscitation in patients with traumatic
function in critically ill patients with acute kidney brain injury. New England Journal of Medicine. 2007;
injury. Kidney International. 2009; 6: 422–427. 357: 874–884.
Bruegger D, Rehm M, Abicht J, et al. Shedding of the Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl
endothelial glycocalyx during cardiac surgery: on- starch or saline for fluid resuscitation in intensive
pump versus off-pump coronary artery bypass graft care. New England Journal of Medicine. 2012;
surgery. Journal of Thoracic and Cardiovascular 367: 1901–1911.
Surgery. 2009; 138: 1445–1447. O’Dell E, Tibby SM, Durward A, Murdoch IA.
Cherpanath TG, Aarts LP, Groeneveld JA, et al. Defining Hyperchloremia is the dominant cause of metabolic
fluid responsiveness: a guide to patient-tailored acidosis in the postresuscitation phase of pediatric
volume titration. Journal of Cardiothoracic and meningococcal sepsis. Critical Care Medicine. 2007;
Vascular Anesthesia. 2014; 28: 745–754. 35: 2390.
Chowdhury AH, Cox EF, Francis ST, et al. A randomized, Perel P, Roberts I. Colloids versus crystalloids for
controlled, double-blind crossover study on the effects fluid resuscitation in critically ill patients.
of 2-L infusions of 0.9% saline and Plasma-lyte® 148 Cochrane Database of Systematic Reviews. 2012;
on renal blood flow velocity and renal cortical tissue 2012(6): CD000567.
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Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl Tollofsrud S, Noddeland H. Hypertonic saline and
starch 130/0.42 versus Ringer’s acetate in severe sepsis. dextran after coronary artery surgery mobilises
New England Journal of Medicine. 2012; 367: 124. fluid excess and improves cardiorespiratory
Raghunathan K, McGee WT, Higgins T. Importance of functions. Acta Anaesthesiologica Scandinavica. 1998;
intravenous fluid dose and composition in surgical 42: 154–161.
ICU patients. Current Opinion in Critical Care. 2012; Woodcock TE, Woodcock TM. Revised Starling equation
18: 350–357. and the glycocalyx model of transvascular fluid
Shaw A, Raghunathan K. Fluid management in cardiac exchange: an improved paradigm for prescribing
surgery: colloid or crystalloid? Anesthesiology Clinics. intravenous fluid therapy. British Journal of
2013; 31: 269–280. Anaesthesia. 2012; 108: 384–394.
MCQs
1. The main determinant of fluid disposition after car- 4. Regarding physiologically balanced solutions:
diopulmonary bypass is: (a) They can cause hyperchloraemic metabolic acidosis
(a) Total volume of fluid given (b) Their use is associated with maintenance of renal
(b) Electrolyte composition blood flow
(c) Endothelial glycocalyx integrity (c) Administration of physiological solutions is an

acid-base intervention
(d) The patient’s intravascular fluid status
(d) They are preferred to colloids in cardiac surgical
(e) Serum albumin level patients
2. Fluid responsiveness in the postoperative cardiac sur- (e) Their use is contraindicated in hypoalbuminaemic
gical patient is assessed by: patients
5. Regarding colloids in the cardiothoracic ICU:
(a) Increase in central venous pressure
(a) Their use has been associated with impairment of
(b) Increase in stroke volume
the blood-brain barrier
(c) Increase in mean arterial pressure
(b) Starch solutions can cause acute kidney injury and
(d) Decrease in lactate levels should be avoided
(e) Increase in urine output (c) Albumin has a role in hypoalbuminaemic patients
3. Fluid overload in the cardiothoracic critically ill: with clinical tissue oedema
(a) Is associated with poor clinical outcomes (d) They are the fluid of choice to assess fluid
responsiveness
(b) Is associated with acute kidney injury
(e) The incidence of anaphylaxis relating to use of gela-
(c) Is associated with postoperative acute respiratory tin solutions is 0.04%
distress syndrome (ARDS)
(d) Is associated with prolonged mechanical ventilation
(e) Is associated with late graft dysfunction in lung
transplant recipients
14:08:11
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123
Inotropes and Vasopressors

Chapter
15 Gabriel Kleinman, Shahzad Shaefi and Charles Shayan
Introduction (Figure 15.1). The end result is vascular smooth mus-

cle constriction. This leads to globally increased sys-
Ahlquist’s discovery in animal models of two distinct
temic vascular resistance (SVR). In the perioperative
types of adrenergic receptors in 1948 set the founda-
setting, A1r agonists are used to counter the decreased
tion for the modern day critical care use of inotropic
SVR seen with a variety of physiological and patho-
drugs. He named these receptors in relation to their
physiological processes. The A1r does not undergo
activity as activators (alpha) or blockers (beta). His
sensitisation, or internalisation, though at maximal
original work has been expanded exponentially by dis-
supratherapeutic agonist doses, it could produce
covery of subtypes of the originally identified recep-
organ ischaemia or substantially increase SVR, which
tors as well as many other discrete types of vasoactive
can be widely distributed in epicardial, renal, splanch-
receptors. Though it was uniquely postulated that
nic, cerebral and pulmonary vascular beds.
these vasoactive receptors respond only to sympathin
(epinephrine), we now know that these G protein cou-
pled receptors (GPCRs) are regulated by a variety of Beta Receptors
agonists and antagonists and play a key role in preva- B receptors (Br) are subtyped into B1, B2 and B3 vari-
lence of sympathetic nervous system activity. In the ants and regulate inotropy and chronotropy as well as
cardiac ICU, these vasoactive receptors are stimulated smooth muscle relaxation in various vascular beds.
with various natural and synthetic molecules, result- Their distribution is not uniform. Although B1r and
ing in augmented cardiac output (CO), chronotropy B2r are both present in myocardium, thoracic aorta
and mean arterial pressure (MAP), and in some and carotid artery, and epigastric and pulmonary
cases enhanced lusiotropy in the postsurgical cardiac artery, B1 is the predominant receptor subtype in the
setting. Norepinephrine, epinephrine, dopamine, myocardium. B1 agonism exerts its effect through the
dopexamine, dobutamine, milrinone, enoximone, Gs GPCR pathway. This interaction in cardiac cells
levosimendan and phenylephrine are the most com- leads to calcium induced calcium release from the
monly encountered vasoactive agents in the intensive myocardial sarcoplasmic reticulum, thereby allow-
care unit. We will review the current evidence for the ing increased actin- myosin cross linkages and an
use of inotropic agents in the perioperative care of car- enhanced chronotropic and inotropic state.
diac patients. In contrast to the action of beta agonists on car-
diac cells, in smooth muscle, B2r stimulation leads
Alpha-1 Receptors to increased activity of cAMP dependent protein
kinase, increased phosphorylation and activation of
Furthering Ahlquist’s work, Piascik elucidated the
phospholamban, increased cellular calcium reuptake
mechanism of action of GPCRs. Upon agonist bind-
through the ryanodine receptors and, ultimately,
ing to the alpha-1 receptor (A1r), Gq protein stimu-
vasodilation.
lates the phospholipase C (PLC) system, which in its
turn activates the 1,2-diacylglycerol (DAG) protein
kinase C (PKC) pathway through hydrolysis. The con- Dobutamine
sequence of this enzymatic process is an increased Dobutamine is a synthetic Br (B1, B2) agonist,
release of calcium from the sarcoplasmic reticu- which entered clinical use in 1978 as a promising
lum (SR) and increased protein phosphorylation replacement for dopamine in the treatment of acute
14:13:54 123
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124
overall metabolic and objective parameters (O2 deliv-

ery and renal perfusion) between the two groups.
Thus, in patients with non-ischaemic HF requiring
inotropic support, dobutamine may be the better
agent compared to epinephrine given the tendency
of epinephrine to aggravate lactic acidosis and, con-
versely, its lower effectiveness in an acidotic milieu.
Though dobutamine infusions are frequently used as
pharmacological therapy for bridge to cardiac trans-
plantation or for long-term management of heart fail-
ure in patients not eligible for transplant, eosinophilic
hypersensitivity reactions have been reported. The
relationship between dobutamine and eosinophilia
appears to be related to dose of dobutamine and dura-
tion of treatment, eventually resulting in eosinophilic
myocarditis with unfortunate further decompensation
of the patient’s underlying cardiac disease. It is well
documented that chronic infusions of dobutamine are
Figure 15.1 β1 receptor: AC adenylyl cyclase, cAMP cyclic associated with higher risk for mortality.
adenosine monophosphate, PDE phosphodiesterase, PKA
phosphokinase A, SR sarcoplasmic reticulum, TnC troponin
C. Please refer to the text for detailed explanation.
Norepinephrine (NE)
The primary endogenous neurotransmitter in humans,
decompensated heart failure. It has a 3:1 B1:B2 ago-
norepinephrine, has a more profound effect at A1r than
nist activity and a trivial alpha-1 effect. Dobutamine
at B1r and B2r at clinically relevant doses. Extensive
is used in clinical practice for the treatment of acute
research has been done focusing on the effects of NE
decompensated heart failure in a dose dependent
in the setting of sepsis, and in clinical practice it has
fashion, usually starting with an infusion of 2–3 μg/
a profound vasoconstrictive effect with less heart rate
kg/min and rapidly uptitrated to a therapeutic dose of
variability when compared to dopamine and epineph-
7.5–15 μg/kg/min. It increases CO, stroke volume and
rine. This finding, along with the decreased mortality
coronary perfusion with minimal pulmonary vascu-
associated with NE as compared to other vasoactive
lar effect. Furthermore it has moderate chronotropy
medications, makes it the gold standard choice in the
as it improves the atrioventricular (AV) conduction.
setting of septic shock. In the cardiac ICU it is used to
Tachycardia has been reported to be more signifi-
increase systolic and diastolic pressures and therefore
cant compared to use of milrinone, hence overall
coronary perfusion pressure, in a variety of vasoplegic
oxygen (O2) consumption may be increased with its
states, thus giving it a favourable cardiac profile com-
use. Dobutamine has a mean plasma half-life of 2–3
pared to dopamine and phenylephrine. It appears that
minutes titratable, though after a 72 hour infusion,
the overall effect of NE on CO is determined through
many patients become resistant to dobutamine, due
the interplay of systemic vascular resistance, heart rate
to tachyphylaxis, with resultant rebound hyperten-
and stroke volume variation (SVV). Patients with a
sion on discontinuation probably due to beta receptor
SVV greater than 8.4% are likely to increase their CO
downregulation and internalisation. Dobutamine has
in response to NE, while those with a SVV less than
been shown to increase myocardial oxygen consump-
8.4% are likely to decrease their cardiac output in the
tion, as well as malignant ventricular arrhythmias, at
same setting. Prolonged infusions of NE may have dir-
any dose. Even though dobutamine improves cardiac
ect toxic effects on cardiac myocytes, though this has
output, it has not been shown to optimise regional O2
only been demonstrated in animal models.
delivery to ischaemic vascular beds that need O2 the
most. A recent randomised controlled trial compar-
ing norepinephrine- dobutamine to epinephrine in Epinephrine (Epi)
patients with acute non-ischaemic cardiogenic shock Epinephrine has a dose dependent affinity for A1r,
requiring inotropic support found no difference in B1r and B2r. At low doses, it acts primarily on B1r,
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Chapter 15: Inotropes and Vasopressors
increasing chronotropy, inotropy and lusitropy. As the endothelium. These receptors couple to Gs which
dose is increased, a profound A1r effect is noted. Epi peripherally increases cAMP, causing vasodilation.
acts to increase coronary blood flow at low doses by At low dose infusions up to 3 μg/kg/min, dopamine
increasing the relative time the myocardium is in dias- stimulates DA1 predominantly and results in vaso-
tole. At higher doses, it acts by increasing diastolic and dilation by increasing the intracellular cAMP (and
therefore coronary perfusion pressure. Epi also acts therefore lowering calcium influx) at the level of vas-
to increase blood flow to the pulmonary vasculature cular endothelium in renal, mesenteric beds. In the
through alpha-1 mediated pulmonary vasoconstric- kidneys, dopamine inhibits the NaCl cotransporter at
tion, and dilates bronchioles through B2 mediated the distal convoluted tubule causing diuresis. Despite
smooth muscle dilation. Levy et al. compared Epi to improving renal blood flow, dopamine has not been
combination norepinephrine- dobutamine in car- shown to improve glomerular filtration rate. At the
diogenic shock patients without acute coronary syn- level of myocardium DA1–DA4 receptors are found
drome and found that although Epi is as effective as mainly in atria. At escalating doses (3–10 μg/kg/min)
norepinephrine- dobutamine at achieving haemo- dopamine binds to these receptors as well as B1r and
dynamic goals, it was also associated with increased causes both chronotropy and inotropy, although it is
rates of lactic acidosis, tachycardia, arrhythmias and not quite clear whether these effects are indirect (via
worsened perfusion to gastric mucosa. Furthermore, presynaptic NE release) or by direct B1r stimulation.
use of Epi in treatment of myocardial depression and At doses higher than 10 μg/kg/min, dopamine binds
low cardiac output syndrome may be associated with to A1r causing peripheral vasoconstriction. A trial
more adverse effects on the end-organ function such comparing dopamine to NE in patients with diagnosis
as kidneys in the postoperative period. of shock found that among the subset of patients with
cardiogenic shock, the rate of death was significantly
Isoproterenol higher in the group treated with dopamine than in the
group treated with NE.
Isoproterenol is a purely synthetic B1 and B2 receptor
agonist at clinical doses. While the B1 effects in cardiac
cells lead to increased inotropic and chronotropic states,
the increased cAMP in smooth muscles of the respira-
Milrinone
While most of the vasoactive medications used in the
tory bronchioles and vasculature leads to bronchodila-
cardiac ICU directly exert their effects on GPCRs, mil-
tion with an increase in lung compliance and decrease
rinone, a bipyridine PDE-3 inhibitor, utilises a novel
in SVR respectively. Isoproterenol is used in the EP
mechanism, and is therefore not subject to receptor
laboratory to induce AV nodal re-entrant tachycardias,
phosphorylation, internalisation of deactivation, and
as well as to initiate Wolff–Parkinson–White (WPW)
thus does not demonstrate the need for therapeutic
syndrome re-entry and to chemically pace patients in
dose escalation due to tachyphylaxis. Milrinone exerts
third degree heart block, a property that is very useful
its inotropic effect by inhibiting the conversion of
in heart transplants particularly at the time of separa-
cAMP to AMP, which causes smooth muscle relaxa-
tion from CPB. Experimentally, isoproterenol is used to
tion in peripheral vasodilation, while in cardiac cells
induce acute myocardial infarctions and HF due to the
increased cAMP causes increased lusitropy and inot-
myocardial ischaemia it induces during long infusions.
ropy (Figure 15.2). Due to its lack of receptor internal-
isation and downregulation, like direct B2r, milrinone
Dopamine can be used in a beta receptor depleted state, such
Dopamine is the immediate in vivo precursor to nor- as stage D heart failure awaiting heart transplant.
epinephrine. The actions of dopamine are mediated Milrinone has been shown to improve diastolic dys-
by five distinct GPCRs (D1– D5). These receptors function and increases flow in coronary artery bypass
are found in various densities on the surface of cells grafts after cardiopulmonary bypass, however this
in the nervous system, pulmonary artery, splanchnic effect is not demonstrable if milrinone is given prior
circulation and renal tubules. Dopamine-1 receptors to initiation of cardiopulmonary bypass. On the other
(DA1) are found in the proximal convoluted tubules, hand if milrinone is administered in inhaled fashion
ascending loop of Henle and collecting ducts. DA2 prior to initiation of CPB it is beneficial in the first
receptors are mainly located in the renal vascular 24 hours postoperatively in cardiac patients with
14:13:54 125
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126
considered an inotrope. Animal studies initially dem-

onstrated that dopexamine may have immunomod-
ulatory effect (B2 interaction), notably decreased
lactataemia and cytokine release in animal models
of endotoxaemia. This effect has not been duplicated
in clinical observations. Dopexamine was compared
to dobutamine in a randomised double blind, cross-
over fashion, in a paediatric population undergoing
cardiac surgery for non-complex congenital correc-
tion, for separation from CPB and mitigating myocar-
dial stunning. Both agents had a similar increase in
CI. Obviously patients treated with dopexamine had
lower systemic vascular resistance (SVR).
Calcium Sensitisers
In normal cardiac cells, tropomyosin and troponin C
Figure 15.2 V1 receptor: DAG diacylglycerol, GDP guanosine (TnC) inhibit the binding of thick to thin filaments.
diphosphate, IP3 inositol triphosphate 3, PIP2 phosphatidylinositol
4,5-biphosphate, PKC phosphokinase C, PLC phospholipase TnC, in the presence of calcium released from the
C. Please refer to the text for detailed explanation. sarcoplasmic reticulum, causes a conformational
change in the troponin-tropomyosin complex, allow-
pulmonary hypertension. The clinical effect of long-
ing extensive thick and thin filament interaction and
term administration of milrinone in ambulatory
thereby myocardial contraction (Figure 15.2). Once
patients was evaluated by Packer who found an exces-
calcium diffuses off its binding site on TnC, tropo-
sive mortality rate in the milrinone treated group.
myosin again returns to its resting position, block-
Milrinone home infusion may be an alternative in
ing the thick and thin filament contractile apparatus.
stage 1B patients awaiting OHT, although the pres-
Under typical physiological conditions, a large cardiac
ence of ICD is advisable given the possibility of ven-
contractile reserve exists. Experimental and in vivo
tricular tachycardia. Milrinone may also be combined
models have demonstrated that increasing calcium
with beta-blockers in stage D heart failure, although
concentration in the sarcoplasmic reticulum leads to
large scale studies still need to be designed to evalu-
increased binding of TnC and, therefore, increased
ate outcomes in these patients. A 2012 meta-analysis
heart rate and inotropic state. It was this contractile
of milrinone treatment in adult cardiac surgery sug-
reserve that led to the development of calcium sensi-
gests that milrinone is associated with a significantly
tising agents that either increase the affinity of TnC for
increased risk of dying when compared with other
calcium or act directly on the thick and thin filaments
drugs (mainly levosimendan). Even though OPTIME-
to allow interaction with little endogenous calcium
CHF investigation showed that milrinone infusion in
required. Two drugs that act to increase the affinity
CHF exacerbation does not improve the mortality, it
of TnC for calcium are currently available outside the
demonstrated that it may have a positive impact on
USA, pimobendan and levosimendan.
renal functions when secondary outcomes were ana-
Pimobendan is an oral agent that exerts its ino-
lysed. However, the full extent of this effect would
tropic effect through calcium sensitising as well c-
have to be evaluated further.
AMP dependent pathway. It has only been studied in
the EPOCH study in a randomised double blind fash-
Dopexamine ion, which demonstrated a non-statistically significant
Dopexamine is a dopamine analogue that has activity decrease in sudden cardiac death, hospitalisation for
at DA1, DA2, B1r and B2r. It has more significant B2r HF, and death from HF in the pimobendan treatment
activity than B1r and hence, along with DA receptors, group. This study also found significantly decreased
activation leads to cerebral, coronary and renal vaso- adverse cardiac events in the treatment group.
dilation and increased perfusion. Despite its particu- Levosimendan, which has a similar mechanism
lar vasodilatory property, in certain vascular beds it is of action to pimobendan, has been shown not only to
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127
improve inotropy as well as lusitropy, but also to cause cardiovascular homeostasis. Vasopressin receptors
vasodilation by activating ATP dependent K chan- are GPCRs, and there are three subtypes of these
nels on the smooth muscles. Levosimendan has been receptors: V1 is found in vascular smooth muscles;
demonstrated to increase SV and CI by 28% and 39% liver, platelets and most peripheral tissues; V2 is only
respectively, while marginally increasing heart rate found in renal collecting ducts; and V3 is limited to
and meanwhile decreasing the left and right filling the anterior pituitary. Stimulation of the V1 receptor
pressures and systemic arterial pressures when com- leads to vasoconstriction through a mechanism simi-
pared to placebo in a double blind RCT. The LIDO lar to that of alpha-1 receptor agonists, Gq activation
trial, which compared levosimendan to dobutamine, of PLC leading to calcium release from intracellular
demonstrated that levosimendan exerted superior stores (Figure 15.2). This vasoconstriction is apparent
haemodynamic effects and in secondary and post hoc when there is a severe dysregulation of sympathetic,
analyses was associated with a lower risk of death after renin-angiotensin systems. Interestingly, vasopressin
31 and 180 days. In addition, the second Randomized has a vasodilatory effect in the cerebral, pulmonary
Multicenter Evaluation of Intravenous Levosimendan and coronary vascular bed at low doses while increas-
Efficacy (REVIVE II) study showed that patients ing the vascular tone in splanchnic, skeletal and cuta-
with ADHF who received levosimendan in addition neous circulations. Recent studies have shown that a
to standard therapy were more likely to show clini- deficiency in vasopressin exists in some shock states,
cal improvement and less likely to deteriorate than and numerous case studies and small trials show vas-
patients on standard therapy alone. However, there opressin increases arterial pressure in septic shock.
was no significant change in 90 day mortality and The largest randomised prospective controlled study
there were more adverse side effects (tachyarrhythmia was published in 2003 by Dunser and colleagues. In
and hypotension) in the levosimendan group. As the this study, 48 patients with catecholamine-resistant
previous studies had only compared levosimendan to vasodilatory shock were prospectively randomised
placebo, the SURVIVE trial compared levosimendan to receive a combined infusion of vasopressin and
to dobutamine in a double blind RCT in patients norepinephrine or norepinephrine alone to main-
requiring inotropic support for ADHF and found that tain a MAP above 70 mmHg. The vasopressin group
despite an initial reduction in plasma B-type natriu- showed a significant increase in MAP, cardiac index,
retic peptide level in patients in the levosimendan systemic vascular resistance index, and left ventricu-
group compared with patients in the dobutamine lar stroke work index as well as reduced norepineph-
group, levosimendan did not significantly reduce rine requirements and heart rates. Compared with the
all-cause mortality at 180 days or affect any second- norepinephrine group, there was better preservation
ary clinical outcomes. Like milrinone, levosimendan of gut mucosal blood flow and a significantly lower
used in combination with a beta adrenergic antago- incidence of tachyarrhythmias. In survivors of cardiac
nist may have beneficial effects in patients with car- arrest, vasopressin levels have also been demonstrated
diogenic shock who exhibit tachycardia in response to to be higher than in those cardiac arrest patients who
inotropic agents. do not survive, a finding which led to the inclusion of
vasopressin in the ACLS algorithm.
Vasopressin
Pathophysiology of vasoplegia post cardiac surgery Phenylephrine
involves generation of interleukins, decreased endog- The principal alpha agonist used in clinical practice
enous vasopressin and increased production of NO is phenylephrine, which is a direct-acting syntheti-
by endothelial cells. Vasopressin is a peptide synthe- cally derived alpha-1 agonist. It exerts no beta effects
sised by the paraventricular and supraoptic nuclei due to its lack of a hydroxyl group at position 4 on
of the posterior hypothalamus and is released in the its benzene ring and it causes its vasoconstrictive
capillary bed of the posterior pituitary gland where effects through inhibition of cAMP production. In
there is no blood-brain barrier. Its release is potently the perioperative period, it is used to rapidly increase
regulated by plasma osmolality and haemodynamic the mean arterial pressure and maintain forward flow
parameters such as decreased blood pressure produc- in patients with systolic outflow tract obstruction
ing hormones that are essential for osmotic as well as and single ventricle physiology. The rapid increase in
14:13:54 127
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128
MAP caused by phenylephrine can lead to a carotid

baroreceptor-mediated bradycardia. At clinically rel-
Further Reading
Alhashemi JA. Treatment of cardiogenic shock with
evant doses, phenylephrine reduces CO and increases levosimendan in combination with β-adrenergic
myocardial work, and oxygen requirements. Though antagonists. British Journal of Anaesthesia. 2005;
not definitive, this may be associated with myocardial 95: 648–650. doi: 10.1093/bja/aei225
injury and significantly decreased coronary perfusion. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh
In addition to its usefulness as both a bolus and infu- J. Low-dose dopamine in patients with early renal
sion perioperative medication, phenylephrine has also dysfunction: a placebo-controlled randomised trial.
been described in case reports to correct smooth mus- Australian and New Zealand Intensive Care Society
cle vascular tone in patients who coingest both PDE-5 (ANZICS) Clinical Trials Group. Lancet. 2000;
inhibitors and nitrates. 356: 2139–2143.
De Backer D, Biston P, Devriendt J, et al. Comparison
of dopamine and norepinephrine in the treatment
Methylene Blue of shock. New England Journal of Medicine. 2010;
Methylene blue, which is normally used as a cell dye 362: 779–789.
and as a treatment for cyanide poisoning, when given Klein L, Massie BM, Leimberger JD, et al. Admission
as an intravenous bolus or infusion, binds to and or changes in renal function during hospitalization
inhibits guanylate cyclase, scavenges nitric oxide and for worsening heart failure predict postdischarge
inhibits synthesis of nitric oxide via iNOS. All three survival: results from the Outcomes of a Prospective
of these actions lead to decreased systemic levels of Trial of Intravenous Milrinone for Exacerbations
of Chronic Heart Failure (OPTIME-CHF).
cGMP and NO, which act to synergistically mini-
Circulation: Heart Failure. 2008; 1: 25–33.
mise the overall response to endogenous vasodila-
tors. Methylene blue has been used successfully for Laflamme M, Perrault LP, Carrier M, et al. Preliminary
experience with combined inhaled milrinone
the treatment of vasoplegic syndrome, for which fluid
and prostacyclin in cardiac surgical patients with
resuscitation and conventional vasopressors are inef- pulmonary hypertension. Journal of Cardiothoracic and
fective, as well as vasopressor resistant septic shock. Vascular Anesthesia. 2015; 29: 38–45.
Two studies have specifically looked at the role of
Levy B, Perez P, Perny J, Thivilier C, Gerard A. Comparison
methylene blue in cardiac surgery patients at highest of norepinephrine-dobutamine to epinephrine for
risk for developing vasoplegic syndromes (preopera- hemodynamics, lactate metabolism, and organ
tive ACE inhibitors, calcium channel blockers). When function variables in cardiogenic shock. A prospective,
administered in the preoperative period, the treated randomized pilot study. Critical Care Medicine. 2011;
patients had greater haemodynamic stability, less 39: 450–455.
vasopressor requirements, less fluid administration, Majure DT, Greco T, Greco M, et al. Meta-analysis of
fewer blood transfusions, and decreased intensive care randomized trials of effect of milrinone on mortality
unit and overall hospital stays. None of the patients in cardiac surgery: an update. Journal of Cardiothoracic
who received methylene blue developed vasoplegic and Vascular Anesthesia. 2013; 27: 220–229.
syndrome, while 26% of the placebo patients did go Mebazaa A, Nieminen MS, Packer M, et al. Levosimendan
on to develop some degree of vasoplegic syndrome. vs dobutamine for patients with acute decompensated
The same haemodynamic stability and decreased heart failure: the SURVIVE Randomized Trial.
ICU and hospital stay held true for patients that were
297: 1883–1891.
given methylene blue after the development of vaso-
plegic syndrome. Though a rapid and effective treat- Movsesian M, Stehlik J, Vandeput F, Bristow MR.
Phosphodiesterase inhibition in heart failure. Heart
ment for vasoplegic syndrome, methylene blue is not
Failure Reviews. 2009; 14: 255–263.
a completely benign drug. Severe renal impairment
is an absolute contraindication, as it is excreted pre- Nathan Coxford R, Lang E, Dowling S. Dopamine versus
norepinephrine in the treatment of shock. Canadian
dominantly by the kidney. Relative contraindications
Journal of Emergency Medicine. 2011; 13: 395–397.
include G6PD deficiency and other oxidiser initiated
haemolytic anaemias. Methylene blue also inhib- Ozal E, Kuralay E, Yildirim V, et al. Preoperative methylene
blue administration in patients at high risk for
its MAO and must be used cautiously in patients on
vasoplegic syndrome during cardiac surgery. Annals of
SSRIs, who are at a higher risk for serotonin syndrome. Thoracic Surgery. 2005; 79: 1615–1619.
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MCQs
1. A 45 year old male is presenting to CTICU for postop- (a) Milrinone
erative management after a heart transplant. His past (b) Dobutamine
medical history is significant for arrhythmogenic right
ventricular hypertrophy. His immediate postoperative (c) Epinephrine
vitals include a BP = 100/70, HR = 65. (d) Dopamine
What inotropic agent would be MOST appropriate to
(e) Centre dependent
start at this point?
(a) Dopamine 4. A 55 year old patient s/p MVR/TVR/AVR is present-
ing to CTICU. On admission the patient is on infusion
(b) Milrinone
of high dose milrinone, dobutamine and dopamine.
(c) Dobutamine Patient BP = 80/40, HR = 100, CI = 2.1.
(d) Norepinephrine What agent would be the MOST useful to infuse at
this time?
(e) No need for inotropic agent
2. A 65 year patient with longstanding history of CAD is (a) Phenylephrine
presenting to CTICU for further postoperative manage- (b) Norepinephrine
ment. His preoperative systolic and diastolic functions
(c) Epinephrine
are severely reduced.
What would be the LEAST appropriate inotropic agent (d) Vasopressin
in this patient?
5. A 66 year old African American male is presenting
(a) Dopamine s/p heart transplant (complicated intraoperative course),
(b) Milrinone with profound thrombocytopenia and high pyrexia. His
past medical history is significant for anxiety, severe
(c) Dobutamine depression and opioid abuse.
(d) Epinephrine Administration of all the following agents may contrib-
ute to his symptomology EXCEPT:
(e) Levisomendan
(a) Odansetron
3. A 75 year old patient with longstanding history of non-
(b) Fluoxetine
ischaemic cardiomyopathy and chronic heart failure
(CHF), necessitating multiple hospitalisations and vol- (c) Trazadone
ume overload management in the past, is readmitted for (d) Methylene blue
acute exacerbation of his CHF.
What is the MOST desirable inotropic agent to use in (e) Methadone
this patient?
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Sedation and Analgesia

Chapter
16 Lachlan Miles and Barbora Parizkova
Introduction target concentration will be immediately achieved and

maintained by the infusion without needing to wait
Analgesia and sedation are ubiquitous in the man-
the requisite 3–5 half-lives. If the loading dose yields
agement of the intubated ICU patient, and attitudes
a drug concentration more or less than the target con-
towards them have undergone a paradigm shift in
centration, it will still take 3–5 half-lives for steady
recent years. Where once the ICU was viewed as an
state to be reached, but the starting concentration will
extension of the operating room environment, the
be closer to the steady state concentration than if the
‘anaesthetic triad’ of deep sedation, potent analgesia
loading dose had not been given (Figure 16.2).
and neuromuscular blockade is now rarely indicated
beyond the doors of theatre.
The problems of delirium, agitation and pain are
Sedation
intrinsically connected. It is perhaps best to conceptu- Oversedation is an important cause of morbidity in
alise this ‘ICU triad’ as a three-legged stool –if any ‘leg’ the ICU. The initiation of a sedative or analgesic agent
is neglected, the stool cannot function as intended. should not be based on anticipated distress but rather
on that which is perceived by the clinical team at the
bedside.
Infusion Pharmacokinetics In the postcardiac surgery setting, sedation may be
The administration of sedative and analgesic medica- misused to mask a variety of problems without con-
tions in the ICU is frequently via intravenous infusion. sidering the underlying issue (particularly pain). With
When administering any drug via continuous a few exceptions (status epilepticus, raised intracra-
intravenous infusion, a steady state concentration will nial pressure and severe respiratory failure), it is rec-
eventually be achieved, as determined by the dose rate ognised that maintaining light levels of sedation leads
and the clearance of the drug. to improved clinical outcomes (i.e. shorter duration
The time taken for an infusion to reach this steady of mechanical ventilation, decreased length of ICU
state is determined by the half-life of the drug (the stay). Whilst lighter levels of sedation lead to a more
time taken for the plasma concentration of the drug to pronounced physiological stress response, this has not
decrease by 50%). It takes 3–5 half-lives for a drug to been linked to an increased incidence of myocardial
reach steady state. ischaemia.
For agents with a prolonged half-life, an increase Consequently, it is vital to identify the underlying
in the infusion rate is an inefficient means of achieving cause of any distress, rather than resorting to seda-
desired depth of sedation within a short timeframe. tion in the first instance. Anxiety, pain, delirium and
Increasing the infusion rate to a level such that the tar- residual neuromuscular paralysis are amongst the
get concentration is achieved quickly will result in a most common causes in the intensive care setting.
relative overdose if the infusion is allowed to continue A common underlying cause of anxiety amongst
at that rate (Figure 16.1). this population is patient-ventilator dys-synchrony,
To achieve the target concentration of a drug whilst and the adjustment of ventilator settings (despite
maintaining a continuous infusion at a safe dose rate, acceptable blood gas values) may negate the need for
a loading dose is used. sedation.
If the loading dose is sufficient to achieve the tar- Non-pharmacological strategies are equally impor-
get concentration for a given infusion rate, then the tant. Whilst attention must be paid to addressing the
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Chapter 16: Sedation and Analgesia
4.5
Drug concentration (mgl–1)
3.5
2.5
2
A
1.5
B
1
0.5
Time (hours)
2 4 6 8 10 12 14 16
Figure 16.1 The effects of increasing the rate of infusion to achieve a rapid clinical effect with a hypothetical drug with a half-life of
approximately 4 hours. An increase in the infusion rate (from a steady state of 0.5 mg l−1) is performed. The desired clinical effect is achieved
relatively rapidly, within 15 minutes (at a blood concentration of 1 mg l−1). However, due to the prolonged half-life of the drug, the blood
concentration steadily rises over the next 16 hours, a situation which, if left unchecked, will result in a steady state blood concentration
nine-fold that of the original level, with potentially deleterious effects.
cause of agitation and distress, frequent reassurance • Bispectral index (BIS);

and communication is equally important. Regular • State entropy (SE);
family visits, preservation of regular sleep-wake cycles • Auditory evoked potentials (AEP);
and cognitive-behavioural therapies (music therapy, • Narcotrend index (NI);
relaxation therapy) where available should also be • Patient state index (PSI).
incorporated into patient care.
Whilst these have some use in patients who cannot
be clinically assessed (i.e. patients receiving neuro-
Monitoring Sedation muscular blockade), or in whom monitoring of EEG
A variety of different structured, subjective seda- is particularly important (i.e. non-convulsive status
tion assessment scores have been proposed. Of these, epilepticus), it is generally recognised that they are
the Richmond Agitation- Sedation Scale (RASS) inferior to subjective scoring systems in the non-
(Table 16.1) and the Sedation-Agitation Scale (SAS) paralysed, non-comatose patient.
(Table 16.2) are the most psychometrically reliable
(particularly in terms of inter- rater variability) in Planning Sedation
measuring the quality and depth of sedation in adult As previously mentioned, lighter levels of sedation
ICU patients. In direct comparisons, neither of these lead to improved patient outcomes when combined
measures is clearly superior. with effective analgesia. This has led to the advent of
A variety of different devices have been evaluated protocolised sedative-analgesic strategies, whereby
for the objective measurement of cerebral function in the bedside clinician titrates sedation to a set of prede-
the sedated ICU patient. These include: fined goals, guided by routine, structured, subjective
14:31:24 31
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132
Table 16.1 The Richmond Agitation-Sedation Scale (RASS)
Score Classification Description

4 Combative Overly combative or violent; immediate danger to staff
3 Very agitated Pulls on or removes tube(s) or catheter(s) or has aggressive behaviour towards staff
2 Agitated Frequent non-purposeful movement or patient-ventilator dys-synchrony
1 Restless Anxious or apprehensive but movements not aggressive or vigorous
0 Alert and calm
−1 Drowsy Not fully alert but has sustained (more than 10 seconds) awakening with eye contact to voice
−2 Light sedation Briefly (less than 10 seconds) awakens with eye contact to voice
−3 Moderate sedation Any movement (but no eye contact) to voice
−4 Deep sedation No response to voice, but movement to physical stimulation
−5 Unarousable No response to voice or physical stimulation
8
Drug concentration (mgl–1)
B
4
Time (hours)
2 4 6 8 10 12 14 16
Figure 16.2 This graph demonstrates the effects of a loading dose for a hypothetical drug with a half-life of approximately 4 hours. Curve
A demonstrates the effect of no loading dose, and the target steady state of 4 mg l−1 is reached after 4 half-lives. Curve B shows the effect
of a perfectly calculated loading dose –the target steady state is reached immediately, and maintained by the infusion. Curve C shows the
effect of a partial loading dose. The starting concentration is higher, but it still takes 4 half-lives until steady state is reached. Finally, curve
D shows the effect of an excessive load. The starting concentration is extremely high, and takes 4 half-lives to fall to the target steady state
concentration. Drug concentration in mg l−1. (A black and white version of this figure will appear in some formats. For the colour version,
please refer to the plate section.)
assessments. The ability to undertake such intensive period to allow comprehensive, formal assessment
monitoring is dependent on bedside staffing and of underlying neurological function. The use of this
training, but it is effective in orientating practice technique in isolation has met with controversy in the
towards sedation minimisation. literature. If a unit is already practising sedation mini-
Another strategy is the use of daily sedation inter- misation and/or protocolised sedation, the use of DSI
ruption (DSI). This involves ceasing sedation for a offers little benefit.
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133
Table 16.2 The Sedation-Agitation Scale
Score Classification Description

7 Dangerous agitation Pulls at endotracheal tube, tries to remove catheter, climbs over bed rail, strikes at staff, thrashes
side to side
6 Very agitated Does not calm despite frequent verbal reminding of limits, requires physical restraints, bites
endotracheal tube
5 Agitated Frequent non-purposeful movement or patient-ventilator dys-synchrony
4 Calm and cooperative Is calm, awakens easily, follows commands
3 Sedated Is difficult to arouse, awakens to verbal stimuli or gentle shaking but drifts off again, follows
simple commands
2 Very sedated Arouses to physical stimuli but does not communicate or follow commands, may move
spontaneously
1 Unarousable Has minimal or no response to noxious stimuli, does not communicate or follow commands
Despite years of use, the common agents used for side effect profile, with respiratory depression and
sedation (propofol and benzodiazepines) in the ICU systemic hypotension being the major manifestations.
have only recently been assessed by large, randomised These are often seen when benzodiazepines are used
controlled trials, many of which have significant limi- in combination with other sedating agents. All ben-
tations. This renewed interest came about as a result zodiazepines undergo extensive hepatic metabolism
of the introduction of dexmedetomidine. Sodium by cytochrome P450 enzymes, particularly CYP3A4
thiopentone and the other barbiturates are rarely used and CPY2C19. This leads to prolonged action in
outside of neurosurgical intensive care. They will not low cardiac output states due to diminished hepatic
be discussed in this chapter. extraction.
In general, the choice of sedative agent is
driven by: Midazolam
1. The specific clinical circumstances and sedation Midazolam is possibly the most popular of the ben-
goals for the individual patient including zodiazepines, with a relatively short median half-life
haemodynamic compromise and end-organ of 6.6 hours. It rapidly equilibrates across the blood-
impairment; brain barrier, with duration of action of approxi-
2. The pharmacokinetic profile of the agent, mately 30 minutes after a bolus dose. Accumulation
including half-life, context sensitive half-time, in the setting of prolonged infusion is a common
metabolism and active metabolites, clearance and problem, especially in the elderly or in renal and
side-effects; and hepatic failure. Metabolised by CYP3A4 to the equi-
3. Pharmacoeconomic factors and overall cost. potent active metabolite α-hydroxy-midazolam, it
competes with other drugs (particularly fentanyl) for
Benzodiazepines elimination.
These agents act at the α/γ subunit of the GABAA
receptor to produce sedative effects, mostly by enhanc- Diazepam
ing neurotransmitter binding. They exhibit anxiolytic No longer used as an infusion in the ICU setting as it
and skeletal muscle relaxant properties, although their binds to PVC, diazepam has an elimination half-time
sedative-hypnotic effects are not as pronounced as roughly ~20-fold that of midazolam (20–50 hours),
those of some other classes of agent. Cheap and read- leading to gross prolongation of effect relative to other
ily available, there is some evidence that protracted sedatives. This issue is further compounded by its
use can lead to prolongation of mechanical ventila- multiple active metabolites, including desmethyldi-
tion and length of ICU stay, resulting in diminished azepam, n-methyloxazepam and oxazepam. It cannot
popularity especially when sedation is required for be removed by dialysis and is extremely irritant when
more than 96 hours. They all demonstrate a similar extravasated.
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Lorazepam metabolic acidosis, hypertriglyceridaemia, arrhyth-

mia and escalating vasopressor and inotrope require-
More potent than midazolam or diazepam, lorazepam
ments. The risk of PRIS is increased by high infusion
is less lipid soluble, with a slower onset of effect fol-
rates (>70 μg kg−1 min−1) over prolonged periods, but
lowing a bolus dose. Uncommonly used in the ICU
it has been reported with low dose infusion. The inci-
setting relative to midazolam, the major advantage of
dence of PRIS has been estimated to be as high as 1%.
lorazepam is the lack of active metabolites, theoret-
The syndrome is difficult to diagnose as these patients
ically leading to more rapid offset when the drug is
frequently have multiple aetiologies for clinical insta-
ceased, although the elimination half-life is still 8–15
bility. Management involves early recognition and
hours. The clinical effects and duration of action are
cessation of the infusion, followed by supportive care.
still prolonged by hepatic dysfunction. Parenteral
This may not be sufficient to arrest its progress, and
formulations of lorazepam contain propylene glycol,
consequently, PRIS has a mortality of 33% in some
which has toxic effects. Thought initially to only occur
series.
with very high doses, it has been seen with cumulative
doses as low as 1 mg kg−1 day−1, manifesting as renal
dysfunction and metabolic acidosis. Both of these α2-Adrenoceptor Agonists
occur frequently in the postcardiac surgical patient, Frequently used as second line agents, the α2-agonists
and hence propylene glycol toxicity may be over- act on spinal and supraspinal α2-adrenoceptors
looked as a cause. to accelerate the reuptake of adrenaline and nor-
adrenaline into the presynaptic nerve terminal, thus
Propofol mitigating their excitatory effects. This produces a
different quality of sedation to the more traditional
Propofol is an intravenous sedative that has a number
agents, typified by a more arousable state, with less
of useful properties for use in the ICU. It demonstrates
respiratory depression, as well as demonstrating anal-
sedative, hypnotic, anxiolytic, amnestic and anticon-
gesic (and hence opioid-sparing) effects. These agents
vulsant effects, but is not an analgesic. Whilst acting
are rapidly finding a role in the management of the
as a GABAA agonist, it also acts at a number of other
ICU patient with delirium, both intubated and extu-
receptors in the CNS, such as glycine, nicotinic and
bated. However, despite the absence of respiratory
muscarinic cholinergic receptors.
depression, these agents have been known to cause
As a sedative, propofol is characterised by a rela-
loss of oropharyngeal tone at higher doses, and hence
tively rapid offset of action. This is due to its high lipid
close monitoring of patients receiving them is still
solubility and redistribution away from the site of
required to detect airway obstruction. In keeping with
action, but also its unusual hepatic and extra-hepatic
their site of action, the α2-agonists have cardiovascular
clearance. This results in a short context sensitive
side effects, particularly hypotension and bradycardia.
halftime (despite a prolonged duration of infusion),
As a result, α2-agonists are relatively contraindicated
allows for rapid changes in sedation depth and facili-
in patients with haemodynamic instability or rate
tates daily sedation interruptions.
dependent cardiac output.
Despite its many positive qualities, the use of
propofol is not without risk, particularly in the post-
cardiac surgery patient. Similar to other sedative Clonidine
agents, it causes dose dependent respiratory depres- Despite its relatively unfavourable pharmacokinetics
sion, and hypotension due to systemic vasodilation. (with an elimination half-life of 8 hours), clonidine
These changes are more pronounced in the patient can be administered as an intravenous infusion for
with pre-existing circulatory instability. sedation in the ICU. The drug has an α2:α1 selectiv-
The propofol infusion syndrome (PRIS) is caused ity ratio of 200:1, and is classified as a partial agon-
by the inherent mitochondrial toxicity of the drug, ist by some as increasing doses lead to inevitable
and resembles the mitochondrial myopathies. The α1-adrenoceptor stimulation. Because of the relatively
underlying pathophysiology is impaired entry of low α-adrenoreceptor selectivity, a rise in blood pres-
long-chain fatty acids, disruption of fatty acid oxida- sure due to α1 stimulation following a bolus dose is
tion and failure of the respiratory chain. Manifestation not uncommon, followed by a more sustained fall in
is uncommon, but presents with an unexplained blood pressure and heart rate. Rebound hypertension
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can be seen following sudden cessation of high dose theory, impairs weaning from mechanical ventilation,
infusion (>1.2 g day−1). and increases the risk of lower respiratory tract infec-
tion and deep venous thrombosis.
Dexmedetomidine In the long term, the experience of pain, and an
inability to communicate this, is a common source of
The D-stereoisomer of medetomidine, this agent is a
psychological sequelae, even after physical recovery is
relatively recent addition to the ICU sedation arma-
complete. Those patients who have poorly controlled
mentarium, and is frequently used for the man-
pain during their ICU stay have a higher incidence of
agement of severe delirium. The drug has an α2:α1
post-traumatic stress disorder, chronic pain and an
selectivity ratio of 1600:1, and is classified as a full ago-
overall poorer quality of life.
nist. Onset of action is within 15 minutes after starting
an infusion, with peak sedation reached at 60 minutes.
This may be hastened with the use of a loading dose, Monitoring Analgesia
albeit at a greater risk of haemodynamic instability. There has not been the same focus on analgesia moni-
The drug is rapidly redistributed and broken down by toring scales for the ICU patient as there has been
the liver to inactive metabolites, with an elimination on sedation scales in the literature. In many centres,
time of 2–3 hours; however hepatic dysfunction can crude measures such as vital signs are still in use as the
prolong this. Some studies suggest dexmedetomidine primary means of assessing pain. Whilst such tools
offers decreased time to extubation and decreased may be occasionally of use in the more robust patient,
incidence of delirium relative to midazolam. the postcardiac surgical state is frequently typified by
The uptake of dexmedetomidine has been slow haemodynamic disturbance, meaning that the char-
relative to other agents. This is largely because of cost, acteristic nociceptive response of hypertension and
although the aforementioned benefits offered relative tachycardia may not be present despite the patient
to benzodiazepines may represent a cost saving when experiencing pain.
the drug is used routinely. Monitoring scales for analgesia do exist, and the
realisation that pain and agitation are potentially sep-
arate entities implies that clinical staff should employ
Analgesia separate rating scales and pharmacological strategies
The recognition that agitation and pain are separate in their management. In observational studies, the
entities in ICU patients has been incorporated into behavioural pain scale (BPS) (Table 16.3) and critical
recent clinical guidelines. This is an important dis- care pain observation tool (CPOT) (Table 16.4) score
tinction, as the intubated, sedated ICU patient may consistently well on psychometric evaluation. They
still have some awareness and recollection of their can be implemented quickly and have been shown to
experience, but no way of communicating unpleasant improve patient outcome when used routinely.
sensations to clinical staff. Most patients will experi-
ence pain as part of their ICU stay, whether this is due
to tracheal intubation, the postoperative state or pre-
Planning Analgesia
existing conditions. This can have both short-term A complete overview of all the factors in planning
and long-term consequences. an effective analgesic strategy for a critically ill post-
In the short term, pain results in an acute stress operative patient is beyond the scope of this chapter.
response, with increases in circulating catechola- However, some general principles are worthy of dis-
mines, increasing cardiac afterload, heart rate and cussion when planning an analgesic regimen, and
contractility, all of which increase myocardial oxygen have been highlighted in recent consensus guidelines.
consumption. Tissue perfusion may be impaired due 1. A therapeutic plan and goal of analgesia should be
to peripheral vasoconstriction. The release of other established and communicated to care givers.
stress hormones such as glucocorticoids results in 2. Assessment of pain and response to therapy
a hypermetabolic response, with increased rates of should be performed regularly.
lipolysis and glycolysis being compounded by insu- 3. The level of pain reported by the patient is the
lin resistance and hyperglycaemia, with resultant standard for assessment but subjective observation
impaired wound healing. The presence of a catabolic and physiological indicators may be used when
state increases the risk of disuse myopathy, and, in the patient cannot communicate.
14:31:24 35
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Table 16.3 Behavioural pain scale, scores in the range 4–12
Item Description Score

Facial expression Relaxed 1
Partially tightened (i.e. brow lowering) 2
Fully tightened (i.e. eyelid closing) 3
Grimacing 4
Upper limb movements No movement 1
Partially bent 2
Fully bent with finger flexion 3
Permanently retracted 4
Compliance with mechanical ventilation Tolerating movement 1
Coughing but tolerating ventilation for most of the time 2
Fighting ventilator 3
Unable to control ventilation 4
4. Sedation of critically ill patients should only be oxycodone), morphine has formed the mainstay of
commenced after providing adequate analgesia opioid therapy for decades. It has relatively low lipid
and treating reversible physiological causes. solubility, and hence the onset of effect following a
Needless to say, the involvement of a specialist acute bolus dose is between 15 and 3 0 minutes with peak
pain service for those patients with complex or diffi- effect at 45–90 minutes. The drug is metabolised via
cult to treat pain is invaluable (see Figure 16.3). hepatic conjugation into morphine- 3-
glucuronide
(a metabolite with known neurotoxic side effects),
morphine-6-glucuronide (an active metabolite con-
Opioid Analgesia siderably more potent than morphine) and normor-
Currently, opioids are recommended as the first line phine. These metabolites are then excreted unchanged
agents in the management of non-neuropathic pain in the urine, and dose reduction is required in patients
in the critically ill. This is largely because of their rela- with renal and hepatic dysfunction.
tive efficacy and predictable side effect profile. The
analgesic effects of opioids are achieved through the
μ1-receptor, which is found at a variety of spinal and Oxycodone
supraspinal locations. Indeed, pure μ1-receptor stimu- Another phenanthrene similar to morphine, oxy-
lation provides excellent pain relief. However, there is codone is rarely used in the ICU setting due to the
more than one type of opioid receptor, and stimulation expense of the parenteral formulation. However, it
of the μ1-receptor and these additional sites leads to the undergoes hepatic conjugation to inactive or weakly
characteristic acute side effects of respiratory depres- active metabolites, noroxycodone and oxymorphone,
sion, sedation, reduced gut motility and bradycardia, meaning that accumulation in renal failure is not as
and the longer term issues of tolerance, dependence pronounced.
and opioid induced hyperalgesia. Consequently, opi-
oids should always be prescribed with caution, and the Fentanyl
use of non-opioid analgesia considered in all cases. All
Fentanyl is a potent phenylpiperadine, or synthetic
opioids exhibit similar analgesic efficacy and are asso-
opioid. It has onset of action within 3 minutes due to
ciated with similar outcomes (duration of intubation,
lipid solubility 700–800 fold, and potency 100 fold,
length of stay) when titrated to similar endpoints.
compared with morphine. Consequently, bolus doses,
if not administered with caution, have a greater poten-
Morphine tial to cause sedation and respiratory depression.
Based around three benzene rings, and hence clas- In bolus doses, the duration of action (20 minutes)
sified as a phenanthrene (along with codeine and is limited by redistribution away from the effect site.
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Table 16.4 Critical care pain observation tool (CPOT), scores in the range 0–8
Indicator Description Score

Facial expression No muscular tension observed Relaxed, neutral 0
Presence of frowning, brow lowering, orbit Tense 1
tightening and levator contraction
All of the above plus eyelids tightly closed Grimacing 2
Body movements Does not move at all Absence of movement 0
Slow, cautious movements, touching or Protection 1
rubbing the pain site, seeking attention through
movements
Pulling tube, attempting to sit up, moving limbs, Restlessness 2
thrashing, not following commands, striking at
staff, trying to climb out of bed
Muscle tension No resistance to passive movements Relaxed 0
Resistance to passive movements Tense, rigid 1
Strong resistance to passive movements, inability Very tense or rigid 2
to complete them
Compliance with the ventilator (if Alarms not activated, easy ventilation Tolerating ventilator or 0
intubated) movement
Alarms stop spontaneously Coughing but tolerating 1
Asynchrony; blocking ventilation, alarms Fighting ventilator 2
frequently activated
OR
Vocalisation (extubated patients) Talking in normal tone or no sound Talking in normal tone or no 0
sound
Sighing, moaning Sighing, moaning 1
Crying out, sobbing Crying out, sobbing 2
However, with a prolonged infusion, these periph- is desirable, or in those patients at high risk of exces-
eral sites (particularly adipose tissue) may become sive opioid accumulation. However, possibly due to
saturated, leading to a depot of drug and a marked its potency, remifentanil carries a high risk of opioid
increase in half-life once these compartments equili- induced hyperalgesia, and many studies have sug-
brate with the plasma. Fentanyl is often recommended gested a higher incidence of chronic pain after using
in the setting of renal impairment due to the relative remifentanil in the operative setting, including in car-
lack of active metabolites. The accumulation of nor- diac surgery. This risk may also translate to the ICU.
fentanyl has, however, been reported, and is a poten-
tial cause of toxic delirium. Non-opioid Analgesia
Whilst current guidelines recommend opioids as first
Remifentanil line therapy for the management of nociceptive pain
Remifentanil has been used in anaesthetic practice in the ICU, multiple other classes of analgesic agents
for a number of years. An extremely potent opioid, exist. These drugs are useful, for two reasons:
remifentanil has a unique metabolic pathway, being 1. Minimisation of opioid dose, and hence opioid
rapidly metabolised by plasma esterases. This lim- related side effects; and
its the redistribution of the drug to peripheral com- 2. Management of pain that is not responsive to
partments and keeps the half-life of the drug at 4–5 opioids.
minutes, regardless of the duration of the infusion. It is assumed that the mechanism of action and side
Consequently, it is ideal for those patients in whom effect profile of commonly used drugs such as para-
rapid weaning of sedation to assess neurological status cetamol and the non-steroidal anti-inflammatories are
14:31:24 37
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Anaesthetic and surgical handover from theatre

Actively rewarm if temperature < 36 ºC
Is patient at high risk of severe post-operative pain Optimise cardiac output
(i.e. opioid tolerant, history of substance abuse, history Assess chest tube drainage
of chronic pain)?
Yes No
Administer IV morphine bolus

Commence or continue (0.05–0.1 mg kg–1) unless
opioid infusion patient has already received
(fentanyl or morphine) up to 0.3 mg kg–1 of IV
morphine in the preceding 24
hours
Consider the possible causes for
Administer IV morphine altered level of consciousness
VAS ≤ 3?
bolus (0.05–0.1 mg kg–1) or agitation including inadequate
Stop sedation and assess
analgesia
level of sedation and
analgesia
.018
No Yes
Has patient received adequate Yes RASS 0–1? No

opioid loading (i.e. up to Switch to or maintain oral analgesic regimen:
No
0.3 mg kg–1 of IV morphine) First line: Paracetamol, 1g PO q6h
in the preceding 24 hours?
Second line: Slow release oral opioid BD +
immediate release oral opioid q2 - 4h PRN
14:31:24
Yes Third line: Tramadol PO 1–2 mg kg–1 q8h PRN
Consider alternate analgesic

strategies if appropriate:
Tramadol IV 1–2 mg kg–1
Whilst in ICU, every hour:
PCA opioid (if pain is opioid
responsive) Assess respiratory frequency
Ketamine 0.1 mg kg–1 ± infusion Assess VAS
Monitor analgesic requirements
(particularly opioids)
Monitor chest drain and urine output
Figure 16.3 This algorithm presumes that the patient returns to the ICU on some form of sedation (i.e. propofol, 1–2 mg kg−1 hour−1, and has received some form of opioid loading in the
operating theatre (i.e. morphine bolus, morphine infusion, etc.), and that the patient is receiving regular paracetamol (1 g NG or intravenous q6h). Unless stated otherwise, all medications
should be dosed according to ideal body weight. It is valid only for management of pain in the ICU.
139
well understood, and hence they will not be discussed used in anaesthetic practice, although the use of such
here. However, there are other classes of drug that are a dose in the awake patient increases the risk of side
less commonly used that should be examined. effects. Rapid administration causes nausea and vom-
iting, and hence slow administration over 20 minutes
Ketamine is recommended.
A phencyclidine derivative, ketamine acts via block- In equianalgesic doses, tramadol is far less likely
ade of the n-acetyl-d-aspartate (NMDA) receptor. It to cause respiratory depression than morphine.
effectively has two roles: Respiratory depression has only been observed in
patients with severe renal impairment. Tramadol also
1. Prevention and management of pain due to
has a reputation for provoking seizures. However,
‘central sensitisation’, particularly neuropathic
when given within the recommended dose limits,
pain, severe ‘acute’ pain and opioid resistant
tramadol does not increase seizures relative to other
pain; and
analgesic agents.
2. Reducing the overall dose of opioid required in a
Due to the enhancement of 5- HT release and
given pain situation.
inhibition of reuptake, tramadol is a theoretical
At relatively low doses of 0.1–0.2 mg kg−1 hour−1, cause of serotonergic syndrome. In practice, this is
ketamine acts primarily as an analgesic. Bolus doses rare. Caution should be exercised when prescribing
of 0.1–0.25 mg kg−1 can be used as a loading dose or tramadol in the elderly, in patients with renal impair-
as rescue therapy. Beyond this infusion rate, adverse ment, and with concurrent high doses of serotonergic
effects begin to emerge with relatively little incremen- medications, particularly selective serotonin reuptake
tal analgesic benefit. Vivid dreams and hallucinations inhibitors, noradrenaline-serotonin reuptake inhibi-
are often limiting factors in its use. These effects are tors and monoamine oxidase inhibitors. Note that
entirely dose dependent, and a cessation of the infu- drugs that block the effect of serotonin (particularly
sion will reliably eliminate neurocognitive phenom- the 5-HT3 receptor blockers such as ondansetron) will
ena within the drug half-life of 1–2 hours. The drug is diminish the analgesic efficacy of tramadol.
metabolised to norketamine, an active metabolite that
is renally excreted. Regional Analgesia
At high bolus doses (1–2 mg kg−1), ketamine can First described in 1984, high thoracic epidural anal-
be used to induce anaesthesia. It is often popular in gesia (HTEA) in cardiac surgery has found sporadic
trauma situations as it affords a degree of haemody- acceptance. Proponents argue that the diminished
namic stability relative to other agents by increasing catecholamine release and central neuraxial block-
the peripheral effects of circulating catecholamines. ade attenuates the sympathetic response to the sur-
However, in a state of maximal sympathetic tone, ket- gical insult, leading to a diminished inflammatory
amine cannot increase these effects further, and may response, superior analgesia and earlier postopera-
act as a negative inotrope. Ketamine also preserves tive extubation. It is also argued that the postulated
respiratory drive, although the airway may be compro- risk of epidural haematoma with cardiopulmonary
mised by increased muscle tone and hypersalivation. bypass has not eventuated, provided the epidural is
placed sufficiently in advance of systemic heparini-
Tramadol sation. Depending on the preference of surgeon and
A cyclohexanol derivative, tramadol has a triphasic anaesthetist, patients having cardiac surgery may
mechanism of action. Given intravenously, tramadol occasionally arrive in the intensive care unit with
inhibits the reuptake of noradrenaline and serotonin an epidural catheter in situ, delivering a mixture of
(5-HT), enhancing the action of the descending nox- local anaesthetic and opioid according to local pref-
ious inhibitory control system. In addition, one of its erence. Serious complications of epidural analgesia,
metabolites (M1 or O-desmethyltramadol) is a weak such as epidural haematoma or abscess, will often
opioid agonist. This opioid effect is enhanced with oral manifest with lower limb neurological signs. Hence,
administration due to hepatic first-pass metabolism. sedation should be titrated to allow continuous
Intravenously, tramadol is administered as a bolus assessment of lower limb motor function as the con-
dose of 1–2 mg kg−1 (based on ideal body weight) every sequences of late detection of such a complication are
6 hours. A loading dose of 3 mg kg−1 is occasionally catastrophic.
14:31:24 39
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140
A well- functioning, high thoracic epidural will The association with prolonged weakness has been the
inevitably cause a degree of sympathetic blockade, biggest factor in the decline in popularity of neuro-
which may manifest as hypotension. This can nor- muscular blockade. This phenomenon may be more
mally be managed with judicious intravascular vol- common when aminoglycoside antibiotics or cor-
ume replacement; however, particularly in patients ticosteroids are administered concurrently, because
unable to tolerate further fluid therapy, vasopressors of their interaction at the neuromuscular junction.
may be required. Clinicians may be tempted to stop Spontaneous muscle breakdown during total muscle
the epidural as part of managing hypotension. It is inactivity has also been postulated.
worth noting that the prolonged half-life of the local In practice, neuromuscular blockade can be a
anaesthetic agents commonly used in epidural anal- useful, albeit last line, clinical tool. This is especially
gesia (ropivacaine, bupivacaine and levo-bupivacaine) true in the presence of significant, persistent hypoxia.
means that the benefit of such an action will not be Neuromuscular blockade in this scenario reduces
reaped for some hours, and that it is often best to initi- VO2, and hence reduces tissue perfusion requirements
ate a more definitive plan from the outset whilst con- in skeletal muscle. Patient synchronisation with the
tinuing the epidural. ventilator is also improved.
Regional analgesia is practised commonly in tho- The choice of drug for neuromuscular blockade
racic surgery, where a continuous infusion of local is often clinician dependent; however, the benzyliso-
anaesthetic provides excellent analgesia of the sur- quinoliums (atracurium and cisatracurium) are often
gical site, and minimises the use of oral or intrave- preferred as they undergo organ independent metab-
nous opioid, with the associated risk of respiratory olism. Rather than undergoing hepatic modifica-
depression. For unilateral thoracic surgery where the tion, these drugs are hydrolysed by plasma esterases,
pleura has not been breached adjacent to the verte- or undergo Hoffman elimination. This is a pH and
bral column, many authors advocate a paravertebral temperature dependent process that is prolonged by
block, arguing that the quality of analgesia provided hypothermia and acidosis. The breakdown products
is just as good, with a lower incidence of common of this process (in particular laudanosine) can be neu-
side effects such as hypotension, urinary retention, rotoxic, but at doses well in excess of those encoun-
nausea and vomiting. tered clinically.
Neuromuscular Blockade Further Reading

In the new era of ‘daily sedation interruptions’ and Barr J, Fraser GL, Puntillo K, et al. Clinical practice
‘sedation minimisation’ , the indications for neuro- guidelines for the management of pain, agitation and
delirium in adult patients in the intensive care unit.
muscular blockade (beyond short-term paralysis for
Critical Care Medicine. 2013; 41: 264–306.
invasive procedures such as intubation, bronchoscopy,
Macintyre PE, Scott DA, Schug SA, et al. (Eds). Acute
etc.) in the ICU are limited. Effectively, they can be
pain management in intensive care. Acute Pain
summarised into three categories: Management: Scientific Evidence, 3rd Edition.
1. Facilitation of invasive modes of ventilation, when Melbourne: Australian and New Zealand College of
they are not tolerated by an adequately sedated Anaesthetists and Faculty of Pain Medicine, 2010,
Section 9.8, pp. 286–289.
patient.
2. Open chest: surgical bleeding or indwelling Reade MC, Finfer S. Sedation and delirium in the intensive
care unit. New England Journal of Medicine. 2014;
vascular cannulae may necessitate the patient’s
370: 444–454.
chest being left open for a short time and the
Shehabi Y, Bellomo R, Mehta S, et al. Intensive care
patient being kept completely still.
sedation: the past, present and future. Critical Care.
3. Raised intracranial pressure or status epilepticus. 2013; 17: 322–329.
14:31:24
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MCQs
1. Which of the following represents the ‘ICU triad’ of (d) Diminished haemodynamic perturbation
sedatoanalgesia? (e) Decreased myocardial oxygen demand
(a) Pain, neuromuscular blockade, sedation 4. Which of the following is the superior modality for
(b) Analgesia, sedation, delirium the monitoring of sedation in the standard cardiotho-
(c) Delirium, agitation, pain racic ICU patient?
(d) Agitation, sedation, pain (a) Bispectral index
(e) Analgesia, neuromuscular blockade, sedation (b) Auditory evoked potentials
2. Which of the following determines the time taken for (c) Multichannel electroencephalography
an intravenous infusion of a drug to reach steady state? (d) Richmond agitation-sedation scale
(a) Half-life (e) Glasgow coma score
(b) Clearance 5. Poorly controlled postoperative pain in the ICU set-
(c) Dose rate ting leads to an increased long-term incidence of
which of the following:
(d) Lipid solubility
(a) Major depressive disorder
(e) Molecular weight
(b) Post-traumatic stress disorder
3. Which of the following statements is NOT true? In
general, lighter levels of sedation lead to: (c) Complex regional pain syndrome
(a) Shorter duration of mechanical ventilation (d) Drug induced psychosis
(b) Decreased ICU length of stay (e) Improved quality of life
(c) Increased patient-ventilator dys-synchrony
14:31:24 41
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Mechanical Ventilation
Chapter
17 Anja Schneider and Erik Ortmann
Introduction Limiting Phase
Most patients admitted to the cardiothoracic criti- The limiting variable defines the length or size of
cal care unit will require a form of mechanical ven- inspiratory gas flow. It can also be set to a certain pres-
tilation at some point during their journey. However, sure, volume, flow or time. The type of waveform pro-
the spectrum of indications is wide and ranges from duced for pressure, flow and volume defines a breath
patients on a ‘fast-track’ concept, who are only being delivery. Depending on the chosen limiting vari-
ventilated for a very short period of time directly after able the ventilation pattern may be one of the three
surgery, to very complex patients with severe cardio- following types:
vascular and respiratory failure due to their under-
lying disease or the impact of major cardiothoracic Volume controlled: A constant volume and constant
surgery. Therefore a sound knowledge of the various flow waveform; the pressure waveform will vary
techniques of invasive and non-invasive mechanical depending on lung characteristics.
ventilatory support is essential to develop the appro- Pressure controlled: The pressure waveform has a
priate strategy for the individual patient and their preselected specific pattern but volume and flow
current clinical state. will vary depending on lung characteristics.
Technical Aspects Time controlled: Pressure, volume and flow

The basic principle of modern intensive care ventila- waveforms all vary depending on lung
tors is a positive pressure gradient, which creates gas characteristics.
flow into the lungs during inspiration. Expiration is
usually passive due to fall of the pressure gradient to Cycling Phase
an expiratory level (PEEP). The gas flow is delivered The cycling variable starts the expiration phase by end-
either invasively through an endotracheal tube or a ing inspiratory gas flow. This may also be pressure,
tracheostomy cannula, or non-invasively via a tight volume, flow or time. For example the ventilator may
fitting facemask or similar device. cycle to the expiratory phase after a certain time (i.e.
Traditionally ventilation modes have been preset frequency for mandatory ventilation), when the
described as either volume or pressure controlled. pressure reaches a certain set maximum during inspi-
Modern ventilators however provide a variety of dif- ration, or cycle to the expiratory phase when flow falls
ferent sophisticated modes, some of which combine to a set level (commonly 5 l/min) or percentage (com-
characteristics of both, and are controlled by the so- monly 25%) of peak flow (patient trigger).
called ‘phase variables’ triggering, limiting and cycling. By combining various settings to the different
phase variables, modern ventilators can create a large
Triggering Phase number of ventilation patterns, which can be further
The triggering variable sets the start of inspiratory gas individualised to specific clinical situations. These are
flow and can be time, pressure, flow or volume. Thus all based on three types of breath:
the trigger can be controlled by the ventilator, the A mandatory breath is one in which the ventilator
patient, or a combination of both. When time is the does all the work of breathing and controls the
trigger variable, the breath is considered mandatory. transition between phases of the breath.
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Chapter 17: Mechanical Ventilation
An assisted breath is one where the patient begins no patient effort is detected during a set time
or ‘triggers’ inspiration but the ventilator window, a mandatory inspiration can be triggered
controls the inspiratory phase and the cycling of (time trigger) to guarantee a certain ventilation
inspiration to expiration. frequency.
A spontaneous breath is one in which the patient Respirator triggered: A mandatory breath is
controls the transition between all breathing triggered by set parameters such as inspiratory
phases. time, frequency and I:E (inspiration:expiration)
ratio. The timing is obligatory and the patient has
Ventilation Modes no influence.
Nomenclature of modes of ventilation has become
confusingly complex, with different names being used Expiration
for similar modes by different manufacturers. We want The variable that ends inspiratory gas flow can be
to review the most common terms and explain the either flow or time:
technical principles of the different ventilator modes. Flow cycled: Dependent on the inspiratory flow of
In principle, there are two different techniques of the patient, the expiratory period is triggered as
ventilation: the mandatory technique and the spon- soon as the inspiratory flow has reached a selected
taneous technique. In mandatory modes, ventila- part of the maximum inspiratory flow.
tion is fully or partially controlled by the respirator.
Time cycled: Inspiratory time is defined and
Spontaneous modes allow either independent breath-
expiration begins as soon as a set inspiratory time
ing of the patient or respirator assisted spontaneous
is terminated.
breathing.
Three main subgroups can be classified:
Mandatory ventilation – volume controlled modes
Principles of Mechanical Ventilation
– pressure controlled modes Volume Control Ventilation
Spontaneous ventilation – spontaneous/assisted The parameter remaining constant during this ven-
modes. tilation technique is the tidal volume, which is deliv-
However, this classification is not static and an overlap ered by a constant inspiratory flow. The frequency
with spontaneous/assisted ventilator modes is possi- of the mandatory breaths and the tidal volume can
ble, as the elaborated mandatory techniques can probe adjusted, producing a certain minute volume.
vide assisted or augmented ventilation as well. This is Inspiratory pressure is dependent on patient condi-
an important option, especially during weaning from tions (for example lung mechanics). As patient physi-
mechanical ventilation. Even though modern ventila- ologies vary, it is important to adjust pressure limits
tors have factory presets, to assist application under when using volume control ventilation.
common conditions, a profound understanding of
the control variables is necessary to adjust mechanical Special Feature PRVC and Autoflow®
ventilation to individual patient needs.
Closed loop/servo control modes utilise feedback
monitoring systems within the ventilator to assess
Variables of Mechanical Ventilation breath delivery, compare and contrast the actual
breath delivered with the set target parameters,
Inspiration and then adjust flow and pressure to match these
The inspiration phase is preceded by a triggering phase set parameters more closely. The pressure regulated
during which the ventilator is ‘waiting’ for a signal to volume controlled ventilation (PRVC) combines
start the inspiration. There are two trigger options: a constant tidal volume with the minimum neces-
Patient triggered: Via flow or pressure trigger, sary airway pressure. The inspiratory pressure level
the ventilator identifies the inspiration effort is adapted to lung condition with every manda-
of the patient after which a mandatory breath tory breath. Autoflow® provides additionally the
is delivered. An adjustable trigger threshold possibility of patient triggering during the whole
guarantees individual patient sensitivity. If breathing cycle.
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Pressure Control Ventilation critical care. Therefore different ventilation strat-

egies and ventilation modes need to be applied
Two parameters are remaining constant during pres-
according to the indication but also according to the
sure control ventilation: the lower pressure level (i.e.
clinical phase.
PEEP) and the upper pressure level (i.e. inspiratory
Most patients after cardiac surgery are admitted
pressure). Tidal volume results from patient condi-
to the ICU sedated and mechanically ventilated to
tions, i.e. inspiratory effort, as well as lung mechan-
allow an initial stabilisation phase. Once the patient’s
ics and especially from the difference between the two
clinical situation is deemed stable with regard to car-
pressure levels. The inspiration time determines the
diovascular and respiratory stability, bleeding and
inspiration period and the upper pressure level is con-
coagulopathy, a structured process of weaning from
stant during the whole inspiration time whereas the
mechanical ventilation should be started as early as
decelerating gas flow and tidal volumes are dependent
possible in order to keep the ventilation phase as short
variables
as possible. As soon as sedation reduction has begun,
there should be a protocol based repetitive spontane-
PEEP (Positive End Expiratory Pressure) ous breathing trial, to evaluate muscle weakness and
A positive airway pressure level during the expiration breathing control of the patient. In general, after rou-
period can be achieved by either flow resistance or tine surgery, breathing control and adequate muscle
threshold resistance. Flow resistors work as an expira- strength return quickly.
tory retard device. Pressure across the resistor is regu- However, a proportion of patients experience
lated by flow. Threshold resistors allow continuity of a complex ICU journey with prolonged phases of
expiratory flow until pressure within the breathing mechanical ventilation, and require differentiated
cycle has reached PEEP level (according to threshold strategies. If sedation can be decreased, breath-
value). If possible, ventilators with threshold resist- ing control returns potentially unstable. Breathing
ance technique should be preferred as they reduce muscles may be weak due to critical illness myopa-
resistance during the expiration period and decrease thy and neuropathy. Thus, mixed ventilation modes
the risk of barotrauma. are required, which enable the patient to trigger a
Intrinsic PEEP (or auto-PEEP) is defined as the mandatory breath or in the next step to take spon-
fixed recoil pressure of the respiratory system at end- taneous breaths. Breathing effort is shared between
expiration. It is caused by airway obstruction, or incom- equipment and patient. By the time breathing con-
plete exhalation, which generates flow resistance. trol improves, but muscle weakness is still present,
The application of PEEP may improve ventilation a supported spontaneous breathing mode might be
conditions of the patient and optimise oxygenation adequate. After a long phase of critical illness with
and decarboxylation in different ways, including: ventilator support, a phase of non- invasive ven-
• increase of the functional residual capacity (FRC) tilation (NIV) might be required to stabilise the
with improvement of the alveolar oxygen reservoir, patient’s spontaneous breathing and prevent fur-
• recruitment of collapsed alveoli, which improves ther respiratory failure needing invasive mechanical
lung compliance and reduces pulmonary ventilation.
shunting,
• redistribution of lung oedema from the alveoli to
the interstitium.
Ventilation Modes
However, application of PEEP might also increase CMV (Continuous Mandatory Ventilation)
dead space, increase the risk of barotrauma and
This ventilation mode is ventilator triggered and time
potentially reduce cardiac output. These factors have
cycled. Volume (VC-CMV) or pressure control (PC-
to be taken into account when finding the ‘optimum
CMV) mode is possible. There is no ability to sense
PEEP’ for an individual patient.
patient respiratory effort. This ventilation mode guar-
antees maximum security for controlled ventilation of
Which Mode for Which Patient? a patient, for example directly after admission or for
There is a spectrum of indications for mechanical transport, but requires the patient to be sufficiently
ventilation in patients admitted to cardiothoracic sedated.
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AC (Assist/Assist-Control Ventilation) defined. A spontaneous breathing attempt is enabled

during the whole breathing cycle synchronised to
This ventilation mode allows the patient triggering of
inspiration and expiration. If the mandatory breath is
a mandatory breath due to sensing mechanisms for
reduced due to synchronisation with expiration, the
patient respiratory effort. Thus, it is a time cycled res-
next mandatory breath is prolonged. Synchronisation
pirator or patient triggered mode. Volume (VC-AC)
with inspiration shortens the expiration period.
or pressure control (PC-AC) is possible. In the case
During spontaneous breathing at PEEP level a
of absence of a patient trigger, a mandatory breath
pressure support can be applied. In the case of absence
will be automatically applied after end of expiration.
of a patient trigger during the inspiration trigger
Dependent on patient breathing, this respirator mode
period, a mandatory breath will be delivered.
performs an assist mode or assist-control mode.
This is one of the most common ventilator modes
in modern ICU treatment. Tidal volume, and in con-
SIMV (Synchronised Intermittent sequence minute volume, change based on lung resist-
Mandatory Ventilation) ance and compliance (i.e. patient conditions) and have
This ventilation mode is ventilator or patient con- to be carefully monitored.
trolled and time cycled. The mandatory breaths are
synchronised with the patient’s inspiration effort. PSV (Pressure Support Ventilation)
The defined SIMV rate determines the SIMV cycle. If This ventilation mode is patient or ventilator triggered
the triggering effort occurs in a defined time slot, a and flow cycled with a backup frequency preset. It is a
mandatory breath is applied. This adjustment avoids pressure control mode (PC-PSV). The patient breathes
alteration of the frequency of the mandatory breaths. spontaneously at PEEP level and every inspiration
Volume (VC-SIMV) or pressure control (PC-SIMV) attempt can be pressure supported. Patient conditions
mode is possible. define time, duration and frequency of the mandatory
breath. In the case of absence of patient triggering,
MMV (Mandatory Minute Ventilation) mandatory breaths at inspiratory pressure level will be
This ventilation mode is ventilator or patient con- delivered.
trolled and time cycled. The patient always obtains
defined minute ventilation. Any successful patient CPAP (Continuous Positive Airway
breath is counted towards this target. Volume (VC-
MMV) or pressure control (PC-MMV, volume guar-
Pressure/Pressure Support)
antee enabled) mode is possible. This ventilation mode requires spontaneous breathing
(SPN-CPAP). It is patient triggered and flow cycled.
Compared to atmospheric conditions, this ventila-
APRV (Airway Pressure Release Ventilation) tion mode enables an increased, continuous pressure
This is a pressure controlled (PC-APRV), ventilator level during the entire breathing cycle. Every inspir-
triggered and time cycled ventilator mode. The patient ation effort triggers a flow cycled mandatory breath.
can breathe spontaneously at inspiration pressure Pressure support or variable pressure support (SPN-
level. Active expiration is induced with short pressure CPAP/PS) and volume support (SPN-CPAP/VS) can
reduction (to the low pressure level), to enable opti- be added dependent on patient conditions (i.e. weak-
mised CO2 elimination. The change between the two ness of respiratory muscles). Backup time cycled fre-
pressure levels is machine triggered and time cycled. quencies of mandatory breaths can be adjusted (i.e.
apnoea ventilation).
BIPAP (Biphasic or Bilevel Positive Airway
Pressure) Special Ventilation Modalities
This ventilation mode is ventilator or patient con-
trolled and time cycled. It is a pressure control mode IRV (Inversed Ratio Ventilation)
(PC- BIPAP), which allows the patient to breathe The inspiration to expiration ratio (I:E) is physi-
between two set pressure levels, i.e. PEEP and inspira- ologically about 1:2. Inversed ratio ventilation means
tory pressure. The number of mandatory breaths is prolongation of the inspiration period to up to four
14:33:29 145
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times the expiration period and is therefore not a are beyond the scope of this chapter. Alveoli located
defined mode of ventilation. The mean airway pres- close to the airways are ventilated by convection, for
sure of the breathing cycle is increased to support the more distant alveoli gas mixing mechanisms such as
re-expansion of the collapsed, non-compliant lung in gas streaming, ‘Pendelluft’, and helical diffusion seem
patients with acute lung injury. A combination with to play a major role. The use of HFV is reserved for
increased PEEP can also be reasonable for patients special indications, such as short intrapulmonary
with acute compromised lung, high FiO2 requirements interventions and newborn RDS syndrome.
and restricted decarboxylation, for example after car-
diac surgery, with a history of COPD or pneumonia.
Please note that besides improving the residual capac- NAVA® (Neurally Adjusted Ventilatory
ity, oxygenation and/or decarboxylation, there is an Assist)
increased risk of barotrauma with IRV. One of the problems in weaning from mechanical
ventilation can be a lack of synchronisation between
HFV (High Frequency Ventilation) the patient’s increasing spontaneous efforts and the
This ventilation mode uses much higher respiratory mechanical assistance of the ventilator, especially in
rates and therefore much lower tidal volumes than the case of severe critical illness myopathy and neu-
conventional mechanical ventilation. There are five ropathy. One attempt to improve this synchronisation
different types: is to move from the common flow or pressure trigger
indicating patient effort and move to the neural level
• HFPPV high frequency positive pressure by capturing the electrical activity of the diaphragm.
ventilation In theory this should allow the patient’s attempt to
• HFJV high frequency jet ventilation breathe to be sensed, even if there is not sufficient
• HFOV high frequency oscillatory ventilation movement of the diaphragm. Therefore neural activ-
• HFFI high frequency flow interruption ity and mechanical ventilation can be synchronised
• HFPV high frequency percussive ventilation. to start an assisted breath earlier and better match
As examples, three more commonly used types of the patient’s spontaneous activity. Only a few ven-
high frequency ventilation will be explained. tilator types offer this feature. A special nasogas-
tric sensor tube has to be placed and synchronised
• HFPPV: use of conventional volume or pressure
with the ventilator sensing, which requires a certain
limited ventilation, low compliance and
routine.
respiratory rates of 60–100/minute with tidal
volumes of 100 to 400 ml (danger of inadequate
tidal volume and air trapping). Differential Lung Ventilation
• HFJV: pulses of high pressure gas flow (tidal Differential or single lung ventilation is a frequently
volume up to 150 ml) are delivered with a used anaesthesia technique in thoracic surgery, with
respiratory rate of 100–600/minute over a increasing indication in cardiac surgery. An example is
specialised endotracheal tube or an attachable minimally invasive mitral valve surgery, which is under-
catheter, which creates an open system for taken using this technique in some centres. Commonly
continuous expiration. used devices are double lumen endotracheal tubes and
• HFOV: during the entire respiratory cycle a bronchial blockers.
special pump mechanism generates an oscillating To date in the ICU setting, differential ventilation
pressure (500 to 3000 cycles/minute). This leads has rarely been applied.
to positive pressure during the inspiration period Differential ventilation can be divided into ana-
and negative pressure during the expiration phase, tomical and physiological lung separation. Its ICU
which in contrast to the above modes creates indications can be summarised in the treatment of
active expiration. Mean airway pressure and FiO2 severe unilateral lung disease (after trauma) or lung
determine oxygenation, whereas decarboxylation disease with an asymmetrical distribution (pneu-
is influenced by the oscillatory amplitude. monia, unilateral oedema), aspiration and broncho
The mechanisms of ventilation and oxygenation in pleural fistula. Differential lung ventilation offers the
these ventilation modes are not fully understood and opportunity to use different levels of PEEP, inspiratory
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pressure and volumes. Optimised inspiration to expi- The reduced cardiac output of the right ventricle
ration ratio, and even different gas mixtures to the two leads to a decrease in left ventricular (LV) preload.
lungs can be provided. Even though LV contractility remains unaffected,
the LV compliance and filling might be affected by
Non-invasive Ventilation (NIV) increased intrathoracic pressure due to direct effects
and ventricular interdependence. However, patients
This ventilation mode offers mechanical ventilation
with LV failure still benefit from positive pressure ven-
support without any artificial endotracheal airway
tilation and PEEP (see NIV-CPAP therapy) as it may
(i.e. endotracheal tube, tracheostomy). A variety of
reduce work of breathing and pulmonary oedema.
masks and even helmets are available.
Renal and splanchnic blood flow might be affected
Spontaneous breathing and the patient’s ability to
by positive pressure ventilation and intracranial pres-
protect the airway are mandatory. Most commonly
sure may rise due to reduced venous drainage.
used is the CPAP ventilation mode, with or without
Dependent on patient conditions and ventilation-
pressure support. Indications are acute respiratory
perfusion ratio, PEEP reduces intrapulmonary shunt
failure due to decompensated heart failure with pul-
but potentially increases alveolar dead space. Thus an
monary oedema, exacerbated COPD and obstructive
adequate modification and regular evaluation of PEEP
sleep apnoea.
level is important.
High flow nasal oxygen therapy is worth mention-
ing. This technique delivers heated and humidified
oxygen with a continuous flow over a specialised nasal Effects on the Respiratory System
cannula. Advantages are the creation of a constant Mechanical ventilation can have detrimental effects
positive airway pressure, a reduction of oxygen dilu- on the lung itself, especially if it is needed for pro-
tion and a minimised dead space. longed periods or if an ‘invasive’ ventilation strategy
with high peak airway pressures, high tidal volumes
Physiology of Mechanical Ventilation and high FiO2 is used. Even though mechanical ven-
tilation probably is not the sole cause of respiratory
Cardiovascular System and Circulation complications in a complex intensive care setting, two
The technique of positive pressure ventilation, today conditions have been described in that context: venti-
quite obligatory combined with PEEP, may create lator associated pneumonia (VAP) and ventilator asso-
adverse side effects in the cardiovascular system. ciated lung injury (VALI). Lung infections developing
Positive pressure ventilation, as well as PEEP, lead to after more than 48 hours of mechanical ventilation
an increased intrathoracic pressure and a continu- are usually referred to as VAP and have a significant
ously changing lung volume, both affecting the car- impact on outcome.
diovascular system. The exact mechanisms leading to ventilator asso-
Cardiac output depends on four varia- ciated lung injury (VALI) are still unclear. VALI is
bles: preload, afterload, contractility and heart rate. mostly associated with a pre-existing pulmonary dis-
Generally, the increased intrathoracic pressure, and ease. Important effects are alveolar overexpansion due
especially PEEP, lead to a decrease in cardiac output to high tidal volume (volutrauma), and barotrauma
(CO). This causes reduced venous return and there- because of high airway pressures and prolonged alve-
fore a reduction of right ventricular (RV) preload as olar atelectasis (atelectrauma). Inflammation of the
well as an increase in RV afterload due to increased alveolar tissue and the potential toxicity of high FiO2
pulmonary vascular resistance especially at higher levels may play a role as well (biotrauma).
levels of PEEP (>10–15 cmH2O). The effects on RV Several strategies for protective ventilation have
preload are more pronounced in the presence of been established to prevent VAP (ventilator care bun-
hypovolaemia and autonomic neuropathy. Variation dle) and VALI:
of the systolic arterial blood pressure between the • low tidal volume (maximum 5–7 ml/kg);
inspiratory and expiratory periods of positive pres- • adequate PEEP level and limitation of peak
sure ventilation, usually referred to as ‘pulse pressure inspiratory pressure, pressure support ventilation;
variation’, can even be used to predict the patient’s • IRV (for example protocol based in case of
fluid responsiveness. increasing FiO2 and hypercapnia);
14:33:29 147
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• permissive hypercapnia; The majority of patients requiring invasive venti-

• disinfectant oral care (avoidance of mucosal lator therapy for more than 2 weeks develop serious
drying, secretion retention); critical illness neuropathy and myopathy. Protocol
• airway humidification; based sedation breaks, standardised weaning strate-
• elevated head; gies and a periodically conducted delirium screen can
• cuff pressure monitoring, subglottic suction; help to reduce patient ventilator time.
• minimal sedation strategy;
• early protocol driven weaning from ventilation. Further Reading
Anantham D, Jagadesan R, Tiew PE. Clinical
review: independent lung ventilation in critical care.
Effects on Other Physiological Systems Critical Care. 2005; 9: 594–600.
Gut distension and dysmotility are common during Gattinoni L, Protti A, Caironi P, Carlesso E. Ventilator-
invasive ventilation. Both bleeding and ischaemia induced lung injury: the anatomical and physiological
of the GI tract due to injury of the mucosal wall can framework. Critical Care Medicine. 2010;
occur. Protocolised feeding tube management in com- 38: S539–S548.
bination with stepwise enteral food intake and assess- Skjeflo GW, Dybwik K. A new method of securing the
ment of gastric motility should be applied. airway for differential lung ventilation in intensive care.
The prolonged requirement of sedation to facilitate Acta Anaesthesiologica Scandinavica. 2014; 58: 463–467.
a complex ventilator strategy can also have adverse Yamakawa K, Nakamori Y, Fujimi S, et al. A novel
effects including the risk of delirium. technique of differential lung ventilation in the critical
care setting. BMC Research Notes. 2011; 4: 134.
MCQs
1. Which phase variables in a modern ventilator define a (c) Improvement in lung compliance
pressure controlled ventilation? (d) Reduction in cardiac preload, especially in hypo-
(a) Trigger phase volaemic patients
(b) Limiting phase (e) Reduction of peak airway pressure
(c) Cycling and limiting phase 4. The following ventilator mode is NOT appropriate
(d) Trigger and limiting phase for a patient admitted to the ICU after uncomplicated
aortic valve replacement:
(e) Cycling phase
(a) BiPAP
2. Pressure regulated volume controlled ventilation
(PRVC) provides the following feature(s): (b) HFJV
(a) Constant volume with peak and plateau (c) CPAP/PS

pressure levels (d) SIMV
(b) Constant pressure with variable tidal volume (e) VC-CMV
(c) Pressure controlled ventilation 5. Protective ventilation does NOT include the following
(d) Set tidal volumes with minimum necessary pressure strategy:
(e) Tidal volume adjusted to a minimum airway (a) Adequate PEEP level

pressure (b) Airway humidification
3. Positive end expiratory pressure (PEEP) does NOT (c) Low tidal volume (10–12 ml/kg)
have the following effects: (d) Elevated bed-head
(a) Recruitment of collapsed alveoli (e) Early protocol driven weaning from ventilation
(b) Increase of the functional residual capacity (FRC)
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Renal Replacement Therapy

Chapter
18 Jonah Powell-Tuck, Matt Varrier and Marlies Ostermann
Introduction Types of Renal Replacement Therapy

Acute kidney injury (AKI) is a common compli- There are several techniques of administering RRT,
cation of cardiovascular surgery affecting >20% which can be classified according to the technique used
of patients. The aetiology is complex and includes (modalities) and the duration of therapy (modes).
ischaemia-reperfusion injury, pro-inflammatory pro-
cesses following prolonged cardiopulmonary bypass, Modalities
haemodynamic instability, haemolysis, nephrotoxins
Renal replacement therapy can be administered either
and radiocontrast dye. It commonly develops on the
by utilising an extracorporeal circuit containing an arti-
background of pre- existing comorbidities such as
ficial membrane (haemodialysis or haemofiltration) or
vascular disease, older age and chronic kidney dis-
by utilising the abdominal cavity and the patient’s own
ease (CKD). Following cardiac surgery, patients are
peritoneal membrane (peritoneal dialysis).
particularly vulnerable to the consequences of AKI,
especially electrolyte derangement, metabolic aci- • Haemodialysis (HD) refers to the removal of solute
dosis and fluid accumulation. Between 1 and 5% of and water across a semipermeable membrane by
patients require renal replacement therapy (RRT). means of diffusion across a concentration gradient.
Several risk prediction models for RRT have been Blood is pumped through a filter whilst electrolyte
developed. containing dialysate fluid flows in the reverse
The main indications for starting RRT are: direction on the opposite (non-blood) side of the
filter membrane (see Figure 18.1).
• removal of excess fluid; • Haemofiltration (HF) relies on the principle of
• correction of electrolyte abnormalities (most convection. A pressure gradient is applied across
importantly hyperkalaemia); a semipermeable membrane resulting in removal
• removal of metabolic byproducts (e.g. urea, of solute and water. A balanced replacement fluid
ammonia, sulphates); is added pre-filter and/or post-filter to maintain
• correction of metabolic acidosis; electrolyte concentrations and fluid balance (see
• removal of toxins, including drugs; Figure 18.2). It should be remembered that the
• removal of inflammatory mediators. addition of pre-filter replacement fluid reduces
the delivered RRT dose.
RRT is considered a supportive therapy during a • Haemodiafiltration (HDF) incorporates
period where metabolic and fluid demands exceed the removal of solute and water across a
native kidney function. It can also help to limit non- semipermeable membrane by means of the
renal organ dysfunction that may be exacerbated by application of both a concentration gradient and a
the consequences o f AKI. Although it achieves solute transmembrane pressure (see Figure 18.3).
clearance, acid-base homeostasis and fluid removal, • Peritoneal dialysis (PD) uses the patient’s
it does not fully replace all kidney functions, such as peritoneum as a membrane. Dialysate fluid is
reabsorption of amino acids, activation of vitamin D instilled into the abdominal cavity and drained
and erythropoietin production. out several hours later. Fluids, electrolytes
14:38:13 49
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Figure 18.1 Haemodialysis. (A
black and white version of this figure
will appear in some formats. For the
from paent colour version, please refer to the plate
Blood pump section.)
dialysate
dialysate
to paent
Air detector
Figure 18.2 Haemofiltration. (A black

and white version of this figure will
appear in some formats. For the colour
from paent version, please refer to the plate section.)
Blood pump
Pre-filter replacement fluid
Post-filter replacement fluid

effluent
to paent Air detector
Figure 18.3 Haemodiafiltration. (A
black and white version of this figure
will appear in some formats. For the
from paent Blood pump colour version, please refer to the plate
section.)
Pre-filter replacement fluid
dialysate
dialysate
Post-filter replacement fluid
effluent
to paent
Air detector
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Chapter 18: Renal Replacement Therapy
Table 18.1 Advantages of intermittent and continuous RRT
Continuous RRT Intermittent RRT

Continuous removal of toxins and electrolytes Rapid clearance of toxins and electrolytes
Slower removal of excess fluid (i.e. better haemodynamic tolerability) More time for diagnostic and therapeutic procedures
Less fluid and metabolic fluctuations More time for physiotherapy/rehabilitation
Reduced exposure to anticoagulation
Lower financial costs
Abbreviations: RRT renal replacement therapy.
and small molecules are exchanged across the and haemodiafiltration can be performed as CRRT
peritoneal membrane by diffusion. or IRRT.
HD, HF and HDF should be viewed as equivalent ther- Hybrid therapies such as slow low efficiency dialy-
apies for AKI after cardiac surgery. Middle molecular sis (SLED) or prolonged intermittent renal replace-
weight molecules may be removed more effectively by ment therapy (PIRRT) are variations of RRT, which
convection than by diffusion but there is no evidence are usually provided daily for 6–12 hours. They offer
to suggest that this leads to clinically important differ- the advantages of both intermittent and continuous
ences in outcome. RRT and are often employed during the transition
PD has theoretical advantages in that haemody- period from CRRT to IRRT.
namic disturbance is rare and anticoagulation is not
necessary. However, the efficiency and control of fluid Indications and Timing
and solute balance is inferior to HD, HF and HDF. In In patients with life threatening complications of AKI
chronic PD patients, PD has a role for maintenance such as severe hyperkalaemia, marked metabolic aci-
RRT during the recovery period post surgery. dosis or fluid overload, the decision to urgently start
RRT is generally unequivocal (Table 18.2).
In the absence of overt or impending life threat-
Modes ening complications, the optimal threshold for start-
RRT can be provided intermittently (≈4 hours daily or ing RRT after cardiac surgery remains uncertain.
alternate days) or continuously (24 hours/day). During Important considerations include the severity of ill-
continuous renal replacement therapy (CRRT), solute ness, non-renal organ dysfunction, degree of fluid
clearance and fluid removal occur over a longer time overload, severity of metabolic acidosis, clinical
resulting in less fluctuation in the concentrations of reserve to tolerate fluid overload and metabolic dis-
osmotically active molecules, such as urea and ammo- turbances, anticipated fluid administration and likeli-
nia. Intermittent RRT (IRRT) is more effective at hood of spontaneous recovery of renal function.
clearing small solutes and fluid rapidly. Potential advantages of earlier RRT initiation may
CRRT is recommended for patients who are be offset by the risks of catheter insertion, bleeding,
haemodynamically unstable and/ or do not toler- treatment related haemodynamic instability, infec-
ate rapid fluid removal. It is also superior to inter- tious complications and unwanted losses of nutrients
mittent RRT in patients with cerebral injury or and drugs (Table 18.3). In contrast, delays in initiating
cerebral oedema who may not tolerate fluctuations in RRT may put patients at risk of serious fluid overload
osmotically active molecules. However, the potential and other life threatening complications.
advantages of CRRT are offset by the need for immo- A recent meta-analysis of two randomised con-
bilisation, longer exposure to anticoagulation and trolled trials (RCTs) and nine retrospective cohort
increased health care costs (Table 18.1). Intermittent studies which included a total of 841 patients follow-
RRT has a role in situations where patients are haemo- ing cardiac surgery concluded that the early initiation
dynamically more stable and where the focus of care of RRT was associated with a lower 28-day mortality
has shifted to rehabilitation. and shorter stay in ICU. However, there was marked
Haemodialysis is usually IRRT but can be pro- heterogeneity between the studies including the defi-
vided as CRRT. Haemofiltration is usually CRRT, nitions of ‘early’ and ‘late’ initiation.
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Table 18.2 Summary of absolute and relative indications for starting RRT in critically ill patients with AKI
Absolute indications • Refractory hyperkalaemia (K+ > 6.5 mmol/l or rapidly rising)
• Refractory metabolic acidosis (pH ≤ 7.2)
• Refractory pulmonary oedema due to fluid overload
• Uraemic pericarditis
• Uraemic encephalopathy
• Overdose/toxicity from a dialysable drug/toxin
Relative indications • Progressive fluid accumulation
(in the absence of life threatening • Non-renal organ dysfunction worsened by the effects of AKI
complications of AKI) • Need for large volume fluid administration
• Limited physiological reserve to tolerate the consequences of AKI
• Progressive AKI with little chance of immediate recovery of renal function
• Concomitant accumulation of poisons or drugs which can be removed by RRT
Abbreviations: AKI acute kidney injury; RRT renal replacement therapy.
Table 18.3 Benefits and drawbacks of early RRT
Benefits Drawbacks
Avoidance and/or early control of fluid accumulation and overload Risk of complications associated with dialysis catheter insertion
Avoidance and/or earlier control of complications of uraemia Risk of complications from anticoagulation
Avoidance and/or earlier control of electrolyte/metabolic Risk of haemodynamic instability
derangement
Avoidance and/or earlier control of acid-base derangement Clearance of micronutrients and trace elements
Avoidance of unnecessary diuretic exposure Excess clearance of dialysable medications (i.e. antimicrobials,
antiepileptics)
Clearance of inflammatory mediators Workload for providers
Immobilisation
Healthcare costs
Abbreviations: AKI acute kidney injury; RRT renal replacement therapy.
Clinical practice is often variable. Ideally, the urea generation rate nor volume of distribution can
decision to start RRT should be individualised and be clearly defined. In patients receiving CRRT, the
based on the dynamic context and trajectory of the dose may be estimated considering the effluent flow
patient, illness severity, non-
renal organ dysfunc- rate indexed by the patient’s body weight. It is usually
tion, along with physiological and laboratory data, described as ml/kg/hour.
rather than relying on absolute laboratory values. Based on two large RCTs, the current recommen-
Figure 18.4 shows an algorithm which incorporates dation is to deliver a target dose of 20–25 ml/kg/hour.
these principles. However, unintended interruptions in treatment often
occur which will reduce the effective dose. Therefore,
Dose of RRT doses higher than 20–25 ml/kg/hour may have to be
The dose of RRT is a measure of the quantity of a prescribed but there is no role for high volume RRT.
solute that is removed from the patient during extra- Although the dose of RRT classically refers to
corporeal treatment. In patients on intermittent hae- solute clearance, ultrafiltration rate and target fluid
modialysis, dose of treatment is expressed as urea balance should also be considered as important com-
reduction ratio (URR) or Kt/V (K is dialyser clearance ponents of the prescription. Cardiac surgery results
of urea, t is dialysis time and V is the volume of distri- in an inflammatory state and capillary leak, which
bution of urea). Both parameters have important limi- may result in fluid accumulation. Progressive tis-
tations in critically ill patients with AKI where neither sue and pulmonary oedema can be attenuated by
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AKI Life-threatening complications of AKI

yes
Start RRT
no
Optimise haemodynamic status
Discontinue nephrotoxics if possible
Regular assessment of clinical progress
Persistent AKI and 1 or more of the following:
• progressive fluid accumulation

• cumulative fluid balance >10% of body weight
• worsening metabolic acidosis
• persistent or worsening hyperkalemia yes
Start RRT
• persistent oliguria
• worsening non-renal organ dysfunction
• anticipated large fluid load
• need for administration of nephrotoxins
no
Figure 18.4 Algorithm for deciding whether to begin RRT.
close attention to fluid balance and judicious use of Heparin is still the most commonly used anti-
ultrafiltration. coagulant worldwide; however, the use of citrate for
regional anticoagulation is becoming increasingly
Anticoagulation popular. Citrate acts by chelating calcium, thereby
In patients with AKI requiring RRT, contact of blood inhibiting the clotting cascade at several levels.
with the extracorporeal circuit results in activation Citrate is infused into the circuit prior to the filter
of the coagulation cascade. Additionally, the haem- to achieve an ionised calcium concentration [Cai]
atocrit within the filter increases as a result of fluid of <0.35 mmol/l in blood passing through the filter.
removal, which adds to the risk of the filter clotting. Calcium replacement occurs after the filter to cor-
Premature clotting of the circuit reduces effective rect the calcium deficit in the blood returning to the
clearance, leads to blood loss and increases the work- patient. As a result, the extracorporeal circuit is fully
load and financial costs. The goal of anticoagulation anticoagulated whilst the patient is not. Thus better
is to maintain filter patency, and thus avoid these circuit patency is achieved with fewer bleeding com-
complications. plications. Additionally, citrate serves as a source for
The most commonly used anticoagulation strat- the generation of bicarbonate.
egies include unfractionated heparin delivered sys- Several RCTs and meta- analyses have demon-
temically or via the circuit, low molecular weight strated improved safety, less bleeding complications
heparin (LMWH), systemic epoprostenol, regional and better circuit patency with citrate anticoagulation
anticoagulation with citrate and non-pharmacological when compared to heparin. It is particularly useful in
measures. Other options are thrombin inhibitors such patients with a high bleeding risk, including patients
as argatroban, factor Xa inhibitors such as danapar- in the immediate postoperative period.
oid or fondaparinux, or serine proteinase inhibitors, Non- pharmacological strategies of prolonging
for example nafamostat mesylate. The choice should circuit patency include using higher pump speeds,
be individualised and based on characteristics of the pre-diluting blood with replacement fluid prior to
patient, potential risks and benefits of the anticoagu- the filter or flushing the filter at regular intervals with
lant, availability and local expertise (Table 18.4). saline.
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Table 18.4 Characteristics of commonly used anticoagulants
Characteristics Unfractionated Low molecular Epoprostenol Citrate

heparin weight heparin
Action Inactivation of thrombin Inactivation of Inhibition of platelet Chelation of calcium
and other proteases thrombin and other function
involved in the clotting proteases involved in
cascade the clotting cascade
Extent of Systemic Systemic Systemic Regional
anticoagulation
Most common side Bleeding Bleeding Vasodilation Citrate accumulation
effects HIT HIT metabolic alkalosis
Hypo-/hypercalcaemia
Absolute/relative Bleeding Bleeding Severe haemodynamic Severe liver failure
contraindications HIT HIT instability due to Severe intracellular hypoxia
vasodilation
Abbreviations: RRT renal replacement therapy; HIT heparin induced thrombocytopenia.
Official recommendations by the Kidney Disease: consist of simple discontinuation of RRT, or may
Improving Global Outcomes (KDIGO) expert group include a change in the modality, frequency, or dura-
include the following. For patients not already receiv- tion of RRT. For example, switching from CRRT to
ing effective systemic anticoagulation: IRRT or decreasing the frequency of IRRT from daily
(i) use either unfractionated or low molecular to alternate days are two methods of testing underlying
weight heparin for anticoagulation in patients kidney function.
receiving intermittent RRT; Urine output appears to be the best predictor
(ii) use regional citrate anticoagulation for patients of successful discontinuation. A large prospective
treated with CRRT provided they have no observational study showed that in 529 patients who
contraindications to citrate; survived the initial period of CRRT, 313 were suc-
(iii) use either unfractionated or low molecular cessfully removed from RRT, whereas 216 patients
weight heparin for patients with needed to restart RRT within 7 days of discontinua-
contraindications to citrate receiving CRRT. tion. Multivariate logistic regression analysis showed
that patients who achieved a urine output of greater
Monitoring than 400 ml/24 hours without diuretic use had an
81% chance of successful discontinuation of RRT.
The indication and prescription of RRT needs to be
Patients receiving diuretics with a urine output of
reviewed and adjusted on a daily basis, as the condi-
2330 ml/24 hours had an 87.9% chance of remaining
tion of the patient and treatment goals may change.
off RRT.
This review should include an assessment of the over-
all aims of RRT, the delivered dose, target fluid bal-
ance and filter patency. Particular attention also needs Outcome
to be given to the patient’s drug chart and nutritional The initiation of RRT represents an escalation in both
requirements since RRT affects the clearance of cer- the complexity and costs of care. It is well established
tain medications and is associated with losses of nutri- that the development of AKI is an independent risk
ents and trace elements. factor for in-hospital mortality and this holds true
post cardiac surgery. Patients with severe AKI receiv-
Discontinuation of RRT ing RRT are at increased risk of major morbidity,
RRT should be discontinued when it is no longer including non-recovery of kidney function, rapid pro-
required, either because the patient’s native kidney gression to end-stage renal disease (ESRD) and long-
function has recovered sufficiently to meet the meta- term dialysis dependence, and premature mortality
bolic and fluid demands, or because the goals of care even with recovery of renal function. The risk of ESRD
have changed. The process of stopping RRT may is particularly high in patients with pre-existing CKD.
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Although it is widely recognised that AKI survivors Fortescue EB, Bates DW, Chertow GM. Predicting acute
represent a high risk group, the optimal strategy for renal failure after coronary bypass surgery: cross-
long-term management has yet to be established. validation of two risk-stratification algorithms. Kidney
International. 2000; 57: 2594–2602.
Learning Points Goldstein SL, Jaber BL, Faubel S, Chawla LS. AKI

transition of care: a potential opportunity to detect and
• Patients undergoing cardiac surgery are at prevent CKD. Clinical Journal of the American Society
high risk of AKI including the need for renal of Nephrology. 2013; 8: 476–483.
replacement therapy. Hobson CE, Yavas S, Segal MS, et al. Acute kidney injury
• The indication for renal replacement therapy is associated with increased long-term mortality
should be individualised based on the patient’s after cardiothoracic surgery. Circulation. 2009;
severity and trajectory of illness, degree of fluid 119: 2444–2453.
accumulation, metabolic control and severity of Mehta RH, Grab JD, O’Brien SM, et al. Bedside tool
non-renal organ dysfunction. for predicting the risk of postoperative dialysis in
patients undergoing cardiac surgery. Circulation. 2006;
• Haemodialysis, haemofiltration and
114: 2208–2216.
haemodiafiltration are all acceptable techniques
post cardiac surgery; continuous renal Morabito S, Pistolesi V, Tritapepe L, et al. Regional citrate
anticoagulation in cardiac surgery patients at high risk
replacement therapy is preferred in the setting of of bleeding: a continuous veno-venous hemofiltration
haemodynamic instability. protocol with a low concentration citrate solution.
• The target dose of RRT should be 20–35 ml/kg/ Critical Care. 2012; 16: R111.
hour although this should be adjusted to account Wald R, Quinn RR, Luo J, et al. Chronic dialysis and death
for interruptions to treatment. among survivors of acute kidney injury requiring
• Several techniques to avoid filter clotting are dialysis. Journal of the American Medical Association.
available. Regional citrate anticoagulation offers 2009; 302: 1179–1185.
the best risk-benefit ratio in patients at high risk Wijeysundera DN, Karkouti K, Dupuis JY, et al. Derivation
of bleeding. and validation of a simplified predictive index for
renal replacement therapy after cardiac surgery.
Further Reading 297: 1801–1809.
Bai M, Zhou M, He L, et al. Citrate versus heparin Zarbock A, Kellum JA, Schmidt C, et al. Effect of early vs
anticoagulation for continuous renal replacement delayed initiation of renal replacement therapy on
therapy: an updated meta-analysis of RCTs. Intensive mortality in critically ill patients with acute kidney
Care Medicine. 2015; 41: 2098–2110. injury: the ELAIN randomized clinical trial. Journal
Bastin AJ, Ostermann M, Slack AJ et al. Acute kidney of the American Medical Association. 2016; 315:
injury after cardiac surgery according to Risk/Injury/ 2190–2199.
Failure/Loss/End-stage, Acute Kidney Injury Network, Zhang Z, Hongying N. Efficacy and safety of regional
and Kidney Disease: Improving Global Outcomes citrate anticoagulation in critically ill patients
classifications. Journal of Critical Care. 2013; 28: 389–396. undergoing continuous renal replacement therapy.
Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Intensive Care Medicine. 2012; 38: 20–28.
Lancet. 2012; 380: 756–766. Zou H, Hong Q, Gaosi X. Early versus late initiation
Chertow GM, Lazarus JM, Christiansen CL, et al. of renal replacement therapy impacts mortality in
Preoperative renal risk stratification. Circulation. 1997; patients with acute kidney injury post cardiac surgery:
95: 878–984. a meta-analysis. Critical Care. 2017; 21: 150.
MCQs
1. Which of the following is not an indication for renal (c) Uraemic pericarditis
replacement therapy? (d) Respiratory acidosis
(a) Pulmonary oedema (e) Hyperkalaemia
(b) Metabolic acidosis
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2. Which of the following is an advantage of continuous 4. Which of the following statements regarding antico-
RRT over intermittent RRT? agulation for RRT is correct?
(a) Faster clearance of toxins (a) Citrate inhibits platelet activation
(b) Improved haemodynamic stability (b) Epoprostenol causes vasoconstriction
(c) Reduced exposure to anticoagulation (c) Citrate is recommended as the anticoagulant of
first choice
(d) Improved rehabilitation
(d) Heparin has a better safety profile than citrate
(e) Faster fluid removal
(e) Citrate dose is not titrated against anti-Xa levels
3. Regarding RRT, which of the following statements
is false? 5. Which statement regarding RRT dose is incorrect?
(a) Haemodialysis relies on the principle of convection (a) Following cardiac surgery, higher RRT doses are
associated with decreased 30-day mortality
(b) Haemofiltration removes middle weight molecules
more effectively than haemodialysis (b) In CRRT, dose is estimated as the effluent rate
divided by patient’s weight per hour
(c) In haemodiafiltration, diffusion occurs across the
filter membrane (c) Dose refers to the amount of solute removed from
the patient
(d) Pre-diluting circuit blood can prolong filter
lifespan (d) In intermittent RRT, dose is referred to as urea
reduction ratio
(e) Spontaneous urine output of >400 ml/24 hours
has been associated with successful (e) Interruptions to dialysis will reduce the effective
cessation of RRT delivered dose
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Nutritional Support for Cardiac Surgery

Chapter
19 and Intensive Care
Peter Faber
As most patients after routine cardiac surgery quickly concentration) rarely offer additional information to
resume baseline nutritional intake, specific dietetic a thorough clinical examination and assessment as
assessment and support is rarely required. However, outlined above.
patients with pre- existing malnutrition, especially If additional assessment is required, measure-
underweight, and those requiring prolonged inten- ments of body composition can be applied to meas-
sive care due to perioperative complications are at risk ure body fat content, lean body mass, bone mass and
of further nutritional derangement and early inter- water content. Although some of these techniques,
ventions to optimise nutritional requirements are for example skin fold thickness to measure body fat
recommended. and bioimpedance to measure water, fat and lean tis-
sue, are simple to perform at initial hospital admis-
Nutritional Assessment sion, most methodologies have not been validated for
consecutive measurements in ICU patients. Hence,
At hospital admission patients should be assessed for
wrongly applying such techniques may at best obtain
baseline nutritional status. In the simplest and most
misleading results. Table 19.1 gives normal values for
useful form this includes:
BMI and percentage body fat.
Body weight, height and body mass index (BMI, More accurate methods of estimating body com-
kg/m2); with normal weight defined as a BMI position increase the complexity and may not be use-
between 18.5–24.9 kg/m2; ful in clinical practice. Table 19.2 briefly summarises
Physical examination with an emphasis on muscle the principles behind some methods of estimating
mass and mobility to assess strength and body composition.
coordination;
The presence of oedema, body temperature and oral Normal Nutritional Requirements
health.
For example, elderly patients with poor muscle
Energy Balance
To achieve energy balance (energy intake − energy
strength and oral health will be at increased risk of not
expenditure = energy balance), in a normal healthy
being able to independently feed themselves during
individual an average daily energy intake is required
the recovery period. These patients and the critically
of approximately 2500 kcal for men and 2000 kcal
ill intensive care (ICU) patients are likely to require
for women. It follows that if an individual remains in
either supplementary or full nutritional support.
energy balance, body weight is stable.
To further identify patients at risk of malnour-
ishment, screening questionnaires such as the
Subjective Global Assessment (SGA), Nutritional Energy Intake
Risk Screening (NRS 2002), the Malnutrition The total chemical energy of food (determined by
Universal Screening Tool (MUST) and the NUTRIC bomb direct calorimetry) is not available to the
Score should be used. human body. The energy available to the human body
Unless patients have specific metabolic dis- is termed the metabolisable energy. The difference
eases, biochemical indicators of nutritional sta- in availability of energy is due to not all food being
tus (e.g. plasma transferrin and 3- methylhistidine absorbed from the gastrointestinal tract, the energy
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Table 19.1 Body fat and body mass index
Body fat (%) BMI (kg/m2)

Males Females Normal 18.5–24.9
Normal 12–20 20–30 Overweight 25–29.9
Borderline 21–25 31–33 Obese 30–39.9
Obese >25 >33 Severely obese >40
Table 19.2 Principles of body composition measurements
Method Principle
Imaging techniques (CT, MRI, DEXA scanning) Soft tissue distribution and bone mass can be measured
Density (body plethysmography, under water weighing) Water or air displacement to calculate total body volume and density.
From the density, body composition can be determined. Water has high
density, fat has low density
Bioelectrical impedance (BIA) Electrical resistance varies across the body compartments. Water is a
good conductor, fat less so. Impedance varies with body composition
Stable isotope dilution techniques Tracer isotopes are distributed to specific body compartments. Body
compartment sizes are calculated from volumes and concentrations
Table 19.3 Metabolisable energy and recommended daily intake of macronutrients
Metabolisable energy Recommended daily energy intake, and percentage of total energy
(kcal/g) intake
Carbohydrate 4 No more than 50% (of which free sugars no more than 5%)
Protein 4 0.8 g/kg/day (approximately 15%)
Fat 9 No more than 35% (of which saturated no more than 11%)
costs of metabolism per se, incomplete oxidation of items and, correctly reported and collated, total
protein and energy losses through faeces and urine. energy intake can easily be determined.
Total energy intake is mainly distributed between the
three macronutrients –carbohydrate, fat and protein. Energy Expenditure
Excess energy intake compared with energy expendi- Energy expenditure is more difficult to measure
ture is stored as deposits of glycogen, fat and protein. compared with energy intake. The gold standard for
Fat is the preferential and most efficient way of storing measuring energy expenditure, and hence to ena-
excess energy, as fat tissue has a high energy density ble individually tailored energy intake, is indirect
with low cell turnover. This compares favourably with calorimetry.
carbohydrates, as intracellular glycogen is obligatory Indirect calorimetry is most often applied to meas-
stored with water and protein stores have high energy ure resting metabolic rate (RMR), which is the mini-
costs due to active metabolism and cell turnover. The mum energy required by the body at rest in order to
body has no alcohol storage capacity and thus alcohol fuel essential bodily processes and keep organs and
at 7 kcal/g must be preferentially metabolised before tissues in working order. It is a standardised measure-
the three main macronutrients. ment performed on an awake, supine resting person
Table 19.3 demonstrates the metabolisable energy in a temperature neutral environment after overnight
of the three macronutrients and the recommended fasting (8–10 hours).
daily energy intake. From measurements of oxygen consumption
Total energy intake is measured by recording (VO2), carbon dioxide production (VCO2) and
the amount and composition of food consumed. additional nitrogen excretion it is possible to accu-
Published tables provide the energy content of food rately calculate total energy expenditure as well as
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Chapter 19: Nutritional Support for Cardiac Surgery
macronutrient oxidation (protein, fat, carbohydrates) for lung transplant patients), cardiac patients do not
in health and disease. The most widely used formulae differ from other patients undergoing major surgery
to calculate energy expenditure from indirect calo- and admission to the ICU. Sepsis, stroke, renal failure,
rimetry in humans are those of Elia and Weir: long-term ventilation and bowel ischaemia are feared
perioperative complications across a range of surgical
RMR (kcal/min) = [15.818 VO2 (l/min) + 5.176 specialities as well as for cardiac surgery. These are all
VCO2 (l/min)]/4.18. complications that have a direct impact on the man-
agement of nutritional rehabilitation.
If nitrogen excretion is measured, accuracy is Compared with healthy individuals, the critically
improved by applying ill exhibit an increased turnover and mobilisation of
RMR (kcal/min) = [16.489 VO2 (l/min) + 4.628 stored fuel reserves, especially protein. Due to hor-
VCO2 (l/min) − 9.079 N (g)]/4.18. monal changes and inflammatory response in the ill
patient, this happens even when energy balance has
An assessment of substrate being metabolised can been achieved and thus the resting metabolic rate
be obtained from measurement of the respiratory in what appears to be sedentary ill patients can be
quotient (RQ), which is the volumetric relation- increased by an average of approximately 25% com-
ship between carbon dioxide production and oxygen pared with healthy individuals. In patients with severe
consumption, VCO2/VO2. An RQ approximating 1 burns, RMR can be double baseline value.
indicates carbohydrate oxidation and an RQ approxi- The increase in metabolism caused by the inflam-
mating 0.7 indicates fat oxidation. matory response to surgery and trauma is independ-
Predictive equations, based on age and anthro- ent of the injury type when controlled for the effect
pometry, which negate the requirements for equip- of fever. Fever compounds the increase in metabolism
ment to accurately measure RMR, have been and protein catabolism observed after major surgery,
developed. trauma and sepsis. The resting metabolic rate in these
In health, the Mifflin–St Jeor equation is accurate patients can increase up to 1.5 times compared with
75% of the time when compared with individually healthy individuals. In febrile patients, the meta-
measured indirect calorimetry: bolic rate increases by approximately 10% per degree
RMR (kcal/day) = 10 × weight (kg) + 6.25 × height increase in body temperature and in the most severely
(cm) –5 × age (years) + 5 (males), ill patients energy requirements can reach 40–50 kcal/
kg/day against a normal figure of approximately 25
RMR (kcal/day) = 10 × weight (kg) + 6.25 × height kcal/kg/day. During the acute febrile phase of infec-
(cm) –5 × age (years) –161 (females). tion there is additional salt and water retention, exac-
erbating oedema, renal and ventilatory complications.
In disease, the modified Penn State equation can Thus, although serial measurement of body weight is
be used to account for the metabolic effects of body recommended to monitor energy balance and changes
temperature and minute ventilation: in body weight, in clinical practice it is very difficult to
RMR (kcal/day) = Mifflin × 0.96 + Tmax × 167 + VE accurately weigh intensive care patients, and with the
× 31 − 6212 (males), often concurrent large disturbances in fluid balance,
this is of little added value for assessing nutritional
RMR (kcal/day) = Mifflin × 0.74 + Tmax × 85 + VE × status per se.
64 − 3085 (females). The increased concentrations of cortisol and
catecholamines, and the reduced effect of insulin,
Here Mifflin is the RMR as estimated by the Mifflin–St
compound the often significant protein catabo-
Jeor equation, Tmax is maximum body temperature
lism observed during a sustained inflammatory
(oC) in the previous 24 hours and VE is the minute
response. Urinary nitrogen losses (gram protein
ventilation in litres/minute.
oxidised = 6.25 × gram nitrogen excreted) can be
measured to assess the protein wastage, which in the
Nutritional Requirements in Disease severely ill patient can reach more than 200 g/day. The
Apart from a few exceptions (e.g. cachexia in severe amino acids released from skeletal muscle are used for
mitral stenosis, poor outcome at extremes of BMI gluconeogenesis and protein synthesis, i.e. in disease
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there is an energy increase requiring acceleration of maximum of 2 g/kg/day. If administered as an intra-

protein turnover and enhanced lipolysis. venous lipid emulsion, patients are at risk of meta-
Indirect calorimetry remains the most accurate bolic complications if administered at rates exceeding
method for measuring patients’ energy requirements. 0.11 g/kg/hour. Excessive amount of lipid adminis-
In the absence of this, predictive equations (based on tration results in fat overfeeding syndrome, signs of
the patient’s hospital admission body weight) with addi- which include hypertriglyceridaemia, respiratory
tions for disease pathology will in most cases provide distress, abnormal liver function and coagulopathies.
adequate nutritional support. In clinical practice, how- The calorie content of 10% propofol lipid emulsion is
ever, a value of 25–30 kcal/kg/day is often used as the 1.1 cal/ml and should be included in calculations of
initial energy requirement for most critically ill patients total calorie and fat intake.
Macronutrients Timing and Route of Administration

Protein Enteral Nutrition
Compared with the dietary reference intake (DRI) If the patient is not able to resume full oral intake
of 0.8 g protein/kg/day in healthy individuals, stud- within 24–48 hours, it is recommended to insert a
ies have all demonstrated increased requirement of nasogastric feeding tube to commence full or sup-
protein in critically ill patients. The consensus is to plementary feeding. Cardiothoracic patients should
provide 1.2–1.5 g protein/kg/day with a total energy as a group tolerate enteral feeding and in general
intake from protein approximating 15–20%. If protein there are only very few evidence based contraindi-
is metabolised for gluconeogenesis there is a reduction cations (Table 19.4). It is a common misperception
in skeletal muscle mass as well as structural proteins, that patients in inotrope requiring shock should not
resulting in impaired wound healing and immune receive enteral feeding.
response. In patients with renal failure and increased Enteral nutrition has been demonstrated to be
gastrointestinal losses, protein intake should be re- not only simpler than parenteral nutrition, but also
evaluated and increased. However, in azotaemia and superior in terms of nutritional adequacy, metabolic
ureamia, an excess protein intake can worsen enceph- complications and preservation of gastrointestinal
alopathy in confused patients and patients with integrity. This results in a decreased rate of infection,
intracranial pathology. Hence, judiciously assessed hospital length of stay and organ failure. There is no
protein intake is important for the patients’ recov- firm evidence suggesting the nasogastric feeding tube
ery and although rarely done in clinical practice, the is best placed prepyloric or postpyloric. However, if
measurement of nitrogen balance will improve indi- there are continued large gastric aspirates it may be
vidually determined protein requirements. worth repositioning the feeding tube postpyloric
before commencing parenteral nutrition.
Carbohydrate Although simple in principle, it is often difficult to
The recommended daily intake of carbohydrates (glu- achieve the nutritional requirements by enteral deliv-
cose, oligosaccharides and polysaccharides) is between ery of nutrition and it has been found that only about
2–6 g/kg/day. The optimal amount should be addition- 50% of patients achieve the prescribed nutritional
ally guided by the requirement of protein sparing and intake. Contributing conditions are gastroparesis and
the patient’s ability to metabolise the carbohydrates.
This is done concurrently with insulin administration Table 19.4 Contraindications to enteral feeding
under the guidance of blood glucose (8–10 mmol/l) and Intestinal obstruction or ileus
plasma lactate concentrations. The total daily energy Intractable vomiting/diarrhoea
intake from carbohydrates should be between 30–70%.
Severe gastrointestinal bleeding
Fat Intestinal ischaemia

Severe pancreatitis
Generally fat can safely provide 15–35% of the total
Abdominal compartment syndrome
energy intake. If administered as a lipid emulsion
Gastrointestinal fistula
this equates to approximately 0.5–1.5 g/kg/day with a
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intestinal hypomotility observed in up to 50% of criti- Table 19.5 Proposed enteral reference daily intakes (RDI) of
cally ill patients. This is compounded by for example electrolytes, micronutrients and vitamins
opiates and catecholamines. Nutrient RDI
Impaired gastrointestinal motility is manifest by Sodium 60–100 mmol/day or 1 mmol/kg
abdominal distension and continued gastric residual
Potassium 50–100 mmol/day or 1 mmol/kg
volumes of the delivered nutrition. If impairment
Magnesium 12–14 mmol/day
of gastrointestinal motility prevents adequate calo-
rie intake, supplemental or full parenteral nutrition Phosphate 25 mmol/day
should be considered. A 4–6 hourly gastric residual Calcium 20 mmol/day
volume of between 3–500 ml can be considered as a Zinc 60–190 µmol/day
tolerance indicator to enteral nutrition. Iron 180–270 µmol/day
Feeding should be administered continuously Copper 16–32 µmol/day
and commenced at 20 ml/hour to assess tolerance, Vitamin B12 2–6 µg
and increased in accordance with nutritional require- Vitamin B6 1.5–2 µg
ments and measured gastric aspirates. Therefore some
Folate 180–400 µg
patients may initially not achieve their nutritional
Thiamin 1.2–1.5 mg
goals. Often gastrointestinal motility can be facilitated
by the administration of prokinetic agents, for exam- Vitamin C 60 mg
ple lactulose, erythromycin, metoclopramide and Vitamin A 850–1000 mg
domperidone. Laxatives can be prescribed if there has
been absence of stools for 3 or more consecutive days. If aspirate >250 ml, await nasogastric feeding for
4 hours and aspirate again. Commence feeding
Composition of Enteral Feeds when aspirates <250 ml. Routinely prescribe
Most commercially supplied enteral feeds contain lactulose 15 ml TDS.
1–1.25 kcal/ml. Low volume feeds with the high- If gastric aspirates 250–500 ml, consider
est energy density are used for example for patients administration of:
with renal impairment. Depending on manufac- Metoclopramide 10 mg intravenously TDS
turer, the energy from protein, fat and carbohydrate Erythromycin 200 mg intravenously TDS
is approximately 15– 25%, 25– 35% and 40– 60%, Domperidone 30–40 mg via nasogastric tube.
respectively. If within 3–5 days the patient does not receive >50%
For a standard nutrition formula of 1.2 kcal/ required energy intake, supplementary parenteral
ml, a 75 kg patient would require approximately nutrition should be commenced.
80–100 ml/hour to cover energy and macronutrient
requirements. Parenteral Nutrition
Nasogastric feeds are enriched in electrolytes, For patients in whom enteral nutrition delivers inad-
essential fatty acids, vitamins and micronutrients. In equate calories, supplementary or full parenteral
addition to nutrition, fluid requirements should be nutrition should be commenced. Parenteral nutrition
supplemented by appropriate intravenous or nasogas- is hypertonic and needs to be administered via dedi-
tric fluids, the volume of which should be guided by cated central venous access with formulations sup-
hydration status, renal function and electrolyte bal- plied by the hospital pharmacy after dietetic advice
ance. Daily fluid requirements are approximately and guidance. In well-nourished patients it is not nec-
30–35 ml/kg/24 hours in non-febrile patients. Adult essary to start parenteral nutrition until after 3–5 days
electrolyte, vitamin and micronutrient requirements of failure of attempted enteral feeding.
are shown in Table 19.5. Parenteral nutrition is based upon essential and
Figure 19.1 suggests an algorithm for the initiation non-essential L-amino acids as a source of nitro-
of enteral feeding. gen, glucose for carbohydrates and fatty acids as
Aspirate nasogastric tube before commencing. If no fat. Parenteral formulations are relatively high in fat
aspirate, check that tube is correctly placed by content, alleviating the risk of hyperglycaemia and
chest radiography and/or air insufflation. hepatic steatosis associated with too high an energy
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Start naso-gastric feeding at 20 ml/hr Figure 19.1 Initiation of enteral

Prescribe lactulose TDS feeding.
Aspirate after 4–6 hr
>250 ml No
Yes
Reduce rate by 10 ml/hr Increase rate by 20 ml/hr
Aspirate after 4–6 hr
Increase feeding until calorie demand rate is achieved

Then aspirate only every 6 hr if no complications
equivalent from glucose. Fat can be administered at an increased plasma concentration of triglycerides
a rate of up to 1.2 g/kg/day. Vitamins, trace elements and there is accentuated protein catabolism and aci-
and phosphate are supplemented in appropriate dosis. Renal production and synthesis of hormones
amounts. and amino acids will be impaired during kidney
In clinical practice, there is often a high thresh- injury and renal replacement therapy. Micronutrients
old for commencing parenteral nutrition due to the and water soluble vitamins are often depleted and
recognised complications of hyperglycaemia, infec- should be substituted accordingly. The disturbances
tion, abnormal liver function tests and cholestasis. in fluid balance will add to the complications of clini-
However, by observing judicious antibacterial care, cally assessing nutritional status. Bed bound patients
supplemental insulin administration and frequent receiving renal replacement therapy will experience
review of nutritional requirements, these complica- an accelerated loss of muscle protein in addition to
tions should not prevent the patients from receiv- the clearance of smaller peptides and amino acids by
ing adequate nutrition. It is worth remembering that the haemofiltering membranes. Thus, protein admin-
enteral and parenteral nutrition can often be satisfac- istration should be increased to the order of 1.5–1.8
torily combined, with an overall reduction in compli- g/kg/day. Glutamine becomes conditionally essential
cations associated with either technique. and should be substituted judiciously as should zinc,
phosphorus, selenium and thiamine together with the
Nutrition Adjusted to Renal Failure water soluble vitamins.
Acute kidney injury after cardiac surgery has been
reported to occur in up to 25–30% of patients and a Further Reading
significant proportion of these patients will require Bost RBC, Tjan DHT, van Zanten ARH. Timing of
renal replacement therapy while admitted to the ICU. (supplemental) parenteral nutrition in critically ill
Renal impairment and failure is a common compli- patients: a systematic review. Annals of Intensive Care.
cation that directly affects the nutritional manage- 2014; 4: 31–44.
ment of ICU patients. The metabolism of all three Desai SV, McClave SA, Rice TW. Nutrition in the ICU.
macronutrients is altered, with a decrease in insulin Chest. 2014; 145: 1148–1157.
clearance and glucagon. Changes in the activity of Faber P, Siervo M (Eds). Nutrition in Critical Care.
lipid clearance during acute kidney injury result in Cambridge: Cambridge University Press, 2014.
14:38:49
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Hooper MH, Marik PE. Controversies and misconceptions Ridley E, Gantner D, Pellegrino V. Nutrition therapy in
in intensive care nutrition. Clinics in Chest Medicine. critically ill patients –a review of current evidence for
2015; 36: 409–418. clinicians. Clinical Nutrition. 2015; 34: 565–571.
MCQs
True or False (b) Anti-inflammatory medication will restore a nor-
1. Assessment of nutritional status in patients should mal metabolism
routinely comprise: (c) Grams protein oxidised can be calculated from
(a) Body weight, height and food questionnaires for multiplying urinary nitrogen excretion
total calorie intake 4. In disease the recommended macronutrient intake of
(b) Biochemical markers transferrin and protein, carbohydrate and fat is:
3-methylhistidine (a) Protein intake should be approximately 0.8 g/kg/
(c) Quick and easy measurements of body composi- day providing 15–20% of energy intake
tion, for example bioimpedance and skin-fold (b) Carbohydrate intake should be less than approxi-
thickness mately 1 g/kg/day
2. When discussing energy balance: (c) Fat intake should be approximately 0.5–1.5 g/kg/
(a) Energy intake is easily and simply measured by day
recording food intake into a diary 5. When discussing enteral and parenteral nutrition:
(b) When in energy balance, people losing weight have (a) Feeding should be commenced after 24–48 hours if
a high metabolism and people gaining weight have oral intake has not been resumed
a slow metabolism (b) Postpyloric placement of the feeding tube is prefer-
(c) Basic metabolic rate increases with age able to gastric placement
3. In disease the critically ill patient: (c) The absence or presence of stool guides the initia-
(a) Shuts down the metabolism of amino acids to pre- tion of nasogastric feeding
serve protein
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Physiotherapy and Rehabilitation

Chapter
20 Adam Baddeley and Allaina Eden
Introduction Cardiovascular
Physiotherapy over the last decade has evolved con- • Increased risk of thrombosis
siderably in the areas of critical care, cardiac and tho- • Increased heart rate
racic surgery. This chapter will review the changes in • Reduced blood volume
these areas supported by research, in particular, post- • Orthostatic hypotension
operative critical care based rehabilitation, respiratory • Reduced stroke volume
physiotherapy and physiotherapy practice in relation
to cardiothoracic surgery. Psychological
• Altered mental health (e.g. anxiety, depression,
Rehabilitation PTSD)
• Cognitive issues
Effect of Bed Rest
• Delirium
At some stage during the majority of critical care
admissions, many patients will require sedation to Other
maintain physiological stability during an acute
• Pressure sores/tissue viability
period of illness and will be unable to mobilise out of
• Malnutrition
bed. In addition to sedation and immobility, the use of
neuromuscular blockades and the presence of sepsis • Reduced bone density
lead to intensive care acquired weakness and a reduc-
tion in functional ability. Aims of Rehabilitation
Physical and non- physical changes present in Early rehabilitation is essential to limit the impact
critical care patients. Below are a number of negative of changes associated with prolonged critical care
changes associated with sedation and bed rest, how- stay and should be started as soon as appropriate.
ever, this is not an exhaustive list. Providing treatment to improve the patient’s overall
physical ability is not just the role of the physiother-
Neuromusculoskeletal apist, but requires effective multidisciplinary team
• Muscle atrophy (MDT) working, involving medical and nursing staff,
• Reduced joint range of movement other therapists, the patient’s family, friends and the
• Neuromuscular changes, i.e. the patient. The setting of goals should be discussed and
electromechanical relationship between the nerve agreed with the whole team, including the patient.
and muscle Those involved in rehabilitation can support the
patient to achieve their goals by providing a stimulat-
Respiratory ing environment that encourages independence and
• Reduced respiratory muscle strength maintains focus and orientation for the patient.
The physiotherapist’s role is to coordinate the
• Reduced cough strength
rehabilitation pathway to enable the patient to achieve
• Reduced gas exchange
their goals, and to act as a lead in the provision of
• Reduced ventilation and increased atelectasis
physical rehabilitative treatment. However, other
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Chapter 20: Physiotherapy and Rehabilitation
members of the MDT are crucial in the delivery of is required to identify patients at risk of physical or
rehabilitation, for example, regular functional activi- non-physical morbidity whilst in critical care. Patients
ties such as brushing hair, cleaning teeth, assisting deemed ‘at risk’ should receive comprehensive clinical
with eating, performance of prescribed exercise pro- assessments throughout their hospital admission and
grammes and practising of bed mobility for personal multitherapeutic input.
care. Additional benefits of rehabilitation include a In collaboration with the patient, rehabilitation
reduction in delirium, reduced time weaning from should start as early as possible, based on agreed phys-
mechanical ventilation, reduced length of stay in criti- ical and non-physical rehabilitation goals. These goals
cal care and overall hospital admission, reduction in should be short, medium and long term. Review of
long-term disability and a faster return to normal the assessment should be performed before discharge
functional ability. from critical care, during ward base care, before dis-
charge from hospital and 2–3 months after critical
Early Rehabilitation care discharge. In addition to supportive rehabilitative
in-patient care and community care, follow-up clinics
A large number of research studies on rehabilitation in
provide an environment to identify on-going physical
critical care focus on ‘early’ rehabilitation. Many stud-
and non-physical issues that require referral to other
ies involve services that require referral for physical
healthcare providers. The provision of critical care
therapeutic intervention, therefore the intervention
diaries to patients and their families at follow-up clin-
group receives expedited referrals for rehabilitation.
ics supports patients with memory loss and adjusting
The UK model of healthcare provides the opportu-
to their period of critical illness.
nity for early rehabilitation as physiotherapists assess
respiratory and physical needs at the first assessment.
The research on early rehabilitation supports and rec- Adjuncts and Treatment
ommends that rehabilitation should commence as A standard pattern of exercise progression can be seen
soon as it is safe to do so. This may be passive treat- in Figure 20.1.
ment during times of sedation, or becoming more Some patients require no additional therapeutic
active and participative from the commencement of intervention other than exercise and movement facili-
sedation breaks. tation. However, patients who have received high lev-
Physiotherapy can be provided for patients on els of sedation, paralysing agents and steroids often
mechanical lung ventilation. This can be in the form develop intensive care acquired weakness character-
of stationary bicycles especially adapted to lie on the ised by very poor global muscle power. These patients
bed to early ambulation using a portable ventilator, require increased input to progress. Physiotherapists
and can also be applied to patients on ECMO. have a repertoire of equipment that can be used within
The NICE guidance for ‘Rehabilitation after the critical care environment to aid physical recovery
Critical Illness’ advises that a short clinical assessment and functional ability. Manual handling equipment
Figure 20.1 Pattern of exercise

Non-sedated Alert progression.
Sedated
Poor strength Increasing strength
• Passive range of • Bed or chair based, • Active and
movement bed passive and active resistive/weighted
exercises assisted exercise exercise programme
• Bed bike programme • Standing practice
• Neuromuscular • Hoisting/pat sliding • Stepping practice
electrical stimulation to chair • Standing transfer bed
• Sitting on edge of bed to chair
• Core stability • Marching on spot
strengthening • Walking
• Limb strengthening • Bed/chair cycling or
• Sit to stand practice upright cycle
• Bed or chair cycling
• Tilt table
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such as handling belts, frames, turn aids, standing ensure there are hospital guidelines to ensure this
hoist, tilt table and parallel bars could be used to aid is undertaken safely.
the physical facilitation of patients. However, caution • The key to a successful rehabilitation session is the
should be applied in view of recent surgical wounds, correct staff numbers and skill mix. It is common
i.e. sternotomy and thoracotomy, as it is advised that to require at least two members of physiotherapy
patients should not weight bear through their upper staff (at least one registered physiotherapist) and
limbs during the acute postoperative stage, and tho- the nurse. Additional support from healthcare
racic belts used with some manual handling equip- support workers may be required if moving
ment may be uncomfortable on wounds and drain attachments or a wheelchair is needed.
sites. Pedals that can be used in bed or the chair in
Obtaining enough staff to provide rehabilitation
passive, active assisted or resistive mode have been
throughout the day can be difficult. The use of physi-
shown to increase quadriceps strength and functional
otherapy assistant practitioners to provide some
ability at hospital discharge.
aspects of treatment is a growing practice within criti-
There is emerging evidence that transcutaneous
cal care and ward environments.
neuromuscular electrical stimulation may be ben-
eficial in preserving muscle strength, specifically in
patients who are critically unwell for longer periods, Outcome Measures
and therefore more likely to develop intensive care To assess a patient’s progression throughout their criti-
acquired weakness. The use of interactive video games cal care admission, the regular use of outcome meas-
within critical care can be used to improve muscle ures is strongly recommended. Outcome measures can
strength, balance, coordination and cognitive state. be used to assess level of impairment, physical func-
tional status, mental functional status and neuropsy-
Practicalities and Safety chological functioning. The use of outcome measures
should improve MDT communication, provide
To be able to conduct rehabilitation in critical care
increased direction for treatment planning and help
safely, a number of factors must be considered:
motivate patients. Physiotherapists mainly use meas-
• Assessment of patient’s psychological state, ability ures to evaluate physical changes. There are a multi-
to follow commands and risk/benefit analysis if tude of outcome measures available, however, many do
patient is or becomes delirious during treatment. not have adequate sensitivity to detect small physical
• Does the patient require glasses or hearing aids changes found within debilitated critical care patients.
to be able to participate adequately during the A basic test is the Medical Research Council scale
session? of muscle strength. This is a validated and reliable
• Is the patient receiving or has recently scoring system from 0 (no movement) to 5 (normal
discontinued an infusion of inotropes; is the power). However, this test is not linked to functional
cardiovascular system stable? ability, and therefore its application for a patient’s
• What indwelling cannula, attachments and physical capability is limited.
monitoring does the patient require? What are There are many outcome measures such as Katz’s
the risks if these are disconnected/dislodged Index of Independence in Activities of Daily Living,
during treatment? the Barthel Index, the Rivermead Motor Index and
• What is the patient’s weaning plan? Do they need Functional Independence Measure and Functional
more ventilator support during rehabilitation and Assessment Measure (known as FIM and FAM) which
therefore a plan for treatment before reduction of rank the patient’s ability on functional tasks. However,
support is commenced? these tools lack sufficient sensitivity to recognise small
• If the patient is physically able, it is possible changes in critical care patients’ ability.
to progress rehabilitation to walking whilst Recently developed critical care outcome measures
on the ventilator (this can be achieved with a are Physical Functional Intensive Care test (PFIT) and
tracheostomy or endotracheal tube in situ, if the the Chelsea Critical Care Physical Assessment tool
patient is tube tolerant). (CPAx). PFIT assesses endurance, strength, cardio-
• If the patient is moving outside of the critical care vascular capacity and functional level. The assessment
environment, i.e. to a gym, for rehabilitation, components are: level of assistance required for sit to
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stand, steps per minute whilst marching on the spot,

muscle strength of shoulder flexion and knee exten-
Respiratory Physiotherapy
sion. This tool has proven reliability, validity and Complications of Cardiac and Thoracic
responsiveness. Patients need to be awake and cooper-
ative to complete the PFIT, which is not representative Surgery
of many critical care patients. The volitional aspects of One of the common barriers to recovery following
testing will be dependent on patient effort, which may cardiothoracic surgery is postoperative pulmonary
be poorly performed in critical care. complications (PPCs) which are defined as ‘an identi-
CPAx is a critical care specific tool that is sensi- fiable disease or dysfunction that is clinically relevant
tive enough to recognise small changes in ability in and adversely affects the clinical course’. For patients
patients. It covers 10 dimensions involving respiratory this can lead to an increased length of stay, increased
function, bed and transfer ability and grip strength. morbidity and mortality. The primary role of the
These are graded 0–5 depending on the level of assis- physiotherapist is to aid in preventing PPCs and to
tance required. It is validated for the general adult crit- provide effective treatment to enable a quicker resolu-
ical care population, but not for specialist conditions. tion when they occur.
Examples of common respiratory complications
Barriers to Rehabilitation are:
Despite overwhelming positive evidence in support • Atelectasis or lobar collapse;
of rehabilitation in critical care, treatment is delayed • Sputum retention;
or limited. The Intensive Care Society recommends • Poor cough function due to pain or altered
rehabilitation assessment within 24 hours and 45 min- respiratory mechanics;
utes of rehabilitation per day, 5 days per week by each • Pneumonia;
therapy. In practice, it is difficult to achieve this for • Respiratory failure.
various reasons:
• Staff availability within physiotherapy and Respiratory Physiotherapy –
nursing;
• Respiratory treatments take priority;
What can it Treat?
• Rehabilitation is often time consuming and requires • Reduced lung volumes
higher staff numbers to complete, and therefore is • Sputum retention
not undertaken in times of reduced staffing; • Increased work of breathing (WOB)
• Critical care patients are often too fatigued or • Hypoxia
are having other procedures throughout the day,
which means they are unable to participate in
more than one session per day.
Respiratory Physiotherapy
However, rehabilitation should take place at times Techniques
that are best for the patient. Patients also tend to have
Mobilisation
low motivation to participate in treatment, as there
is little short-term gain, and it is sometimes diffi- Mobilisation is an important treatment for all post-
cult to appreciate how the current treatment leads to surgical patients and should be performed as early as
discharge. possible, ideally the first morning after surgery or even
To overcome barriers, good communication and on the day of surgery. In the early stages, mobilisa-
the setting of daily plans will aid a united approach tion may entail sitting out of bed and/or marching on
to rehabilitation. Providing clear explanation of roles, the spot, with this being progressed to ambulating as
treatment options, anticipated progression and plans soon as is safe for the patient. However, static cycling
will clarify expectations and improve compliance with is equally as effective. The aim of mobilisation is to
patients, their families and staff. Having a clear, docu- increase the tidal volume and minute volume, there-
mented plan for weaning, treatment and rest times fore aiding expansion of atelectatic regions of lung.
ensures patients receive optimal care and achieve their By improving lung volumes and therefore increasing
goals in a timely manner. airflow, secretions are mobilised enabling the patient
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to expectorate more easily. Patients should mobilise at to mobilise, for example a bed bound patient. TEEs
a pace that equates to 3–4 on the Borg scale, or 11– should be performed in the most effective position
14 on the modified Borg scale and on an appropriate for improving lung volumes. The aim of TEEs is to
level of supplementary oxygen if required. Patients improve lung volumes and mobilise secretions by
being ventilated, on inotropes, on extracorporeal increasing tidal volume and using collateral ventila-
membrane oxygenation (ECMO) or ventricular assist tion channels such as the pores of Kohn, communica-
devices (VAD) are not contraindicated to mobilising. tions of Lambert and pathways of Martin.
Each patient should be assessed individually for their
clinical need and safety. Active Cycle of Breathing Technique (ACBT)
Positioning ACBT is a breathing technique using alternating
Positioning is often used in conjunction with other breathing techniques in a cyclical pattern includ-
treatments to help maximise their effectiveness, for ing deep breaths, inspiratory holds, end-inspiratory
example side lying whilst ventilator hyperinflation is sniffs, breathing control, forced expiration technique
performed. It is also an important aspect of patient (FET) and cough. An example of ACBT can be seen in
care in preventing PPCs by positioning patients opti- Figure 20.2. To prevent fatigue a period of breathing
mally in bed or out of bed so as to reduce the time control is used to allow the patient to recover before
spent in recumbent postures such as supine and starting another cycle.
slumped sitting where lung volumes (in particular ACBT can be used in conjunction with postural
functional residual capacity) are naturally reduced. drainage to optimise sputum clearance and also with
An important aspect of positioning is to optimise the ventilator or IPPV to augment the tidal volume
the patient’s ventilation/perfusion (V/Q) matching to further.
improve oxygenation and ventilation. V/Q matching FET can also be varied depending on the position
varies depending on whether the patient is ventilated of the sputum. Low lung volume FET assists with dis-
or breathing spontaneously; this should be considered tal airway sputum whereas high volume FET assists
when positioning the patient. Ventilated patients will with proximal airway sputum.
always have an element of V/Q mismatch due to the ACBT can also be used in conjunction with air-
mechanics of positive pressure ventilation with the way clearance adjuncts such as Acapella, Flutter and
lung tissue and the effects of gravity on the pulmo- OPEP. This provides additional mechanical assistance
nary vasculature. In extreme cases of V/Q mismatch by using a combination of expiratory airflow oscilla-
causing severe hypoxia, prone positioning has proven tions and resistance to provide splinting for airways,
to be beneficial, but is a complicated procedure that in particular for patients with chronic sputum pro-
requires an MDT approach. ducing diseases such as bronchiectasis.
Positioning can also be used to reduce WOB; for
example, forward lean sitting or high side lying. These
Incentive Spirometry (IS)
positions can be used with breathing control tech- Incentive spirometry is the use of a mechanical device
niques for optimal effect. to aid augmentation of tidal volume by providing vis-
Postural drainage uses gravity in specific posi- ual feedback as a motivator. Within the cardiac and
tions to accurately drain certain lobes and segments thoracic surgical population, studies have shown no
of the lungs. These positions can be modified if benefit to the use of IS when compared with early
the patient is unable to tolerate them, for example mobilisation in preventing PPCs; however, they may
head-down tilt. have a role in high risk surgical patients.
Thoracic Expansion Exercises (TEEs)/Deep Breathing Manual Techniques –Percussion, Vibrations

Exercises (DBexs) and Shaking
As with other techniques, TEEs should be used when Manual techniques are rarely used in the cardiotho-
indicated, therefore they should not be used rou- racic surgical patient population due to the incisions
tinely with post cardiac and thoracic surgery patients and potential for causing additional pain and imped-
or as a substitution for patients who can mobilise. ing wound healing. When other airway clearance tech-
TEEs should be used with patients who are unable niques have not been successful, manual techniques
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(b)
(a)
3–5 FET Breathing
and cough control
3–5 deep breaths, end 3–5 deep breaths, end inspiratory

inspiratory sniff +/– 2–3 second sniff +/– 2–3 second inspiratory
inspiratory hold hold
Breathing
control
Figure 20.2 Example of ACBT. (a) Cycle of breathing exercises. (b) Sitting on the edge of the bed rehabilitation with a patient on ECMO.
(A black and white version of this figure (b) will appear in some formats. For the colour version, please refer to the plate section.)
may be useful, with modification of hand position and these pressures up to the required level, normally 20–
force used dependent on wound location. 25 cmH2O. Slow inspiratory flows provide optimal
rise time for deep breathing; however faster flows may
be required for patients who are short of breath with a
Intermittent Positive Pressure Ventilation (IPPV)
high respiration rate.
Also called the ‘Bird’, IPPV is a technique for deliv-
ering positive pressure during the inspiratory phase
via a mouthpiece or facemask to the spontaneously Manual Hyperinflation (MHI)
ventilating patient. A PEEP valve can be applied to MHI is a technique used with patients who have an
the exhalation port to provide airway splinting if artificial airway to augment their tidal volume up
required. An Acapella may be placed on the expira- to 100% of their resting tidal volume, aiming for
tory port to provide airway splinting and expiratory peak inspiratory airway pressures of between 20–
oscillation. Oxygen or medical air can be delivered via 35 cmH2O so that the technique is effective (alveolar
IPPV so that it may be used with patients who are CO2 opening pressures >20 cmH2O) and avoiding baro-
retainers. The use of IPPV requires the patient to be trauma (<40 cmH2O). A manometer should always
able to follow commands and be compliant with treat- be used when performing MHI in combination with a
ment in order to synchronise with the device. IPPV rebreathe circuit using 10–15 l of oxygen. The patient
augments the patient’s tidal volume to aid alveolar should be optimally positioned for the area of lung
recruitment and sputum clearance through collateral that is to be treated, taking into consideration that
ventilation channels. It can also improve the patient’s air takes the path of least resistance and as this tech-
cough through increased tidal volume. IPPV can be nique delivers positive pressure the uppermost lung
used in conjunction with ACBT. in side lying would be preferentially ventilated. This
Typical settings are a low trigger pressure to technique should not be used with patients requir-
enable inspiratory effort without increasing WOB ing a high positive end expiratory pressure (PEEP)
and an inspiratory effort of 10–15 cmH2O, titrating (>10 cmH2O), high FiO2, nitric oxide, high ventilator
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pressures or poor lung compliance, as disconnection treatment optimisation. An example of settings would
from the ventilator would cause a loss of pressure, be an insufflation of 20–25 cmH2O and an exsufflation
lung decruitment and potential sudden hypoxaemia, of −30 to −40 cmH2O. Devices can be set to run in
for example in a patient with acute respiratory distress manual and automated setting modes dependent on
syndrome (ARDS). the treatment requirements.
MHI can be done with a varying technique The mechanism of action for I:E sufflation is through
depending on the aim of the treatment. A combina- provision of an augmented tidal volume on inspiration
tion of slow inspirations with inspiratory pauses and and utilisation of collateral ventilation to reverse atelec-
quick releases of the bag are utilised to improve lung tasis. The sudden swing of pressure into exsufflation
recruitment and sputum clearance. causes shearing forces, which loosens sputum from the
airway walls. The rapid exsufflation with negative pres-
Ventilator Hyperinflation (VHI) sure aids the movement of sputum more proximally so
Studies have shown that MHI and VHI are compara- that it can be either coughed up or suctioned out. It can
ble as treatment techniques with the added safety ben- be used in conjunction with the patient’s own cough
efit of VHI. effort or on its own if a cough is absent.
VHI works through the same mechanisms as MHI
but using adjustment of settings on the ventilator avoids CPAP/NIV/HFNO
disconnection, therefore VHI can be used in patients Other modes of respiratory support may be instigated
with high PEEP requirements. The tidal volume and by a physiotherapist to support the patient in respira-
pressure limits are the same as MHI but with the added tory failure. CPAP and HFNO are used for type 1 res-
benefit of being able to assess lung compliance before piratory failure and NIV for type 2 respiratory failure.
and after treatment, and monitor tidal volume changes
so that effectiveness of treatment and response to the
technique can be measured. Inspiratory pauses are Suction – Endotracheal, Tracheostomy,
also achievable on most ventilators. The concentration Nasopharyngeal, Oral
of oxygen can be maintained at current settings with Suction can be carried out via various artificial airways
VHI, whereas with MHI the flow rate of oxygen and to aid sputum clearance when a patient is unable to
therefore concentration must be increased to allow the do so themselves. A thorough assessment is required
bag to inflate. Depending on mode of ventilation, tidal before suctioning a patient. Indications for suction
volume, inspiratory pressure, set respiratory rate and include retained secretions secondary to:
alarm limits may be adjusted to achieve increased lung
volumes. Guidelines and competency assessment are • Sedation and paralysing agents;
required to ensure safety and standard of practice. • The presence of an artificial airway;
• Ineffective cough secondary to drowsiness;
Manual Insufflation Exsufflation • Pain;
(I:E Sufflation), for example Cough Assist • Ineffective cough secondary to global weakness.
In the author’s opinion, the use of I:E sufflation has The suction technique is the same for each method
become more common within the critical care setting with the only variance being the depth the suction
as the patient population often has problems with a catheter is inserted to. The patient should receive pre-
weakened cough through various mechanisms such oxygenation and postoxygenation to prevent hypoxae-
as pain, anxiety/reduced confidence, altered chest mia. The suction catheter selected should not have an
wall mechanics, phrenic or laryngeal nerve dam- external diameter greater than one-half of the internal
age and intensive care acquired weakness. Manual diameter of the airway. A pressure of −10 to −20 kPa is
I:E can be used on patients with either an artificial recommended with the application of continuous pres-
airway or spontaneously breathing, through a cath- sure rather than intermittent pressure, and no rotation
eter mount or facemask respectively. Oxygen can of the catheter during withdrawal as this has no extra
be entrained into the circuit as required to prevent benefit for sputum removal and can lead to increased
hypoxaemia during treatment. Prior to treatment the mucosal damage. A suction time of no longer than
patient should be positioned optimally. The settings 10–15 seconds is advised as longer is associated with
can be titrated as required for patient comfort and increased risk of mucosal damage and hypoxaemia.
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Respiratory Muscle Training Learning Points

Respiratory muscle training is not commonly used • It is important to consider all of the physiological
in critical care, however there is emerging evidence systems affected and the psychological impact of
within this population that it increases inspiratory being in critical care when rehabilitating critically
muscle strength as assessed by maximal inspiratory unwell patients.
pressure measurements, and may contribute towards • Rehabilitation within critical care should be
expediting the weaning process. commenced as soon as it is clinically safe to do so
to minimise the effects of bed rest.
Considerations for Specific Patient • Rehabilitation is safe to perform on patients in
critical care, and each patient should be assessed
Groups in Critical Care individually for their rehabilitation needs.
• Respiratory physiotherapy is effective at treating
Cardiac diagnosed postoperative pulmonary complications
• Haemodynamic instability can limit the use of in the cardiac and thoracic surgical populations.
some physiotherapy techniques. • The use of prophylactic respiratory physiotherapy
• Adequate analgesia is important for preventing is not recommended or supported by evidence to
PPCs and for enabling patients to be involved prevent postoperative pulmonary complications
with their therapy. in routine, low risk surgical patients.
• Some routine cardiac surgical patients may not
require physiotherapy in critical care if they are
discharged within <24 hours. Further Reading
Berney S, Denehy L. A comparison of the effects of manual
Thoracic and ventilator hyperinflation on static lung compliance
and sputum production in intubated and ventilated
• Enhanced recovery programmes (ERP) are used intensive care patients. Physiotherapy Research
with this patient group and should be followed as International. 2002; 7: 100–108.
soon as possible even in critical care. Brasher PA, McClelland KH, Denehy L, Story I.
• Positive pressure treatment techniques need to be Does removal of deep breathing exercises from a
carefully reasoned due to anastomosis problems. physiotherapy program including pre-operative
education and early mobilisation after cardiac
• Adequate analgesia is important for preventing surgery alter patient outcomes? Australian Journal of
PPCs and for enabling patients to be involved Physiotherapy. 2003; 49: 165–173.
with their therapy.
Gosselink E, Bott J, Johnson M, et al. Physiotherapy for
adult patients with critical illness: recommendations
ECMO of the European Respiratory Society and European
Society of Intensive Care Medicine Task Force on
• Physiotherapists provide treatment for patients on Physiotherapy for critically ill patients. Intensive Care
venovenous (VV) and venoarterial (VA) ECMO. Medicine. 2008; 34: 1188–1199.
• Respiratory physiotherapy techniques can be
Gosselink R, Schrever K, Cops P, et al. Incentive spirometry
limited in these patient groups due to cannulation does not enhance recovery after thoracic surgery.
sites, widespread ARDS and consolidation, Critical Care Medicine. 2000; 28: 679–683.
and low tidal volumes despite high ventilation Hirschhorn AD, Richards DA, Mungovan SF, et al. Does
pressures. the mode of exercise influence recovery of functional
• ECMO patients tend to have the same physical capacity in the early postoperative period after
decline as other critical care patients due coronary artery bypass graft surgery? A randomized
to sedation and bed rest. Therefore early controlled trial. Interactive Cardiovascular and Thoracic
rehabilitation is also essential for this group, with Surgery. 2012; 15: 995–1003.
the additional challenge of ECMO cannulation, NICE. Rehabilitation after Critical Illness. London: NICE,
circuit and limited ventilator reserve. 2009. Report No.: CG83.
• Each ECMO centre has their own protocol with Schweickert W, Pohlman M, Pohlman A, et al. Early
this specialist cohort of patients. physical and occupational therapy in mechanically
14:39:57
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ventilated, critically ill patients: a randomised Warner D. Preventing postoperative pulmonary

controlled trial. Lancet. 2009; 373: 1874–1882. complications. Anesthesiology. 2000; 92: 1467–1472.
Stiller K. Safety issues that should be considered when Zeppos L, Patman S, Berney S, et al. Physiotherapy
mobilizing critically ill patients. Critical Care Clinics. intervention in intensive care is safe: an observational
2007; 23: 35–53. study. Australian Journal of Physiotherapy. 2007;
53: 279–283.
MCQs
1. What pathologies can respiratory physiotherapy treat? (c) Reduced respiratory muscle strength
(a) Reduced lung volumes (d) Reduced cough strength
(b) Sputum retention (e) All of the above
(c) Increased work of breathing 4. At what stage should rehabilitation commence in a
(d) Reduced PaO2 critical care patient?
(e) All of the above (a) Once the patient is no longer sedated
2. Which respiratory physiotherapy technique has no (b) Once cardiovascularly stable

evidence to support its use in routine cardiac and tho- (c) As early as is safe to do so
racic surgical patients? (d) Once agreed by the MDT
(a) Mobilising (e) Once the patient is off the ventilator
(b) Active cycle of breathing techniques 5. For how long should a patient receive rehabilitation
(c) Incentive spirometry from each therapy for the 5 days a week stipulated by
(d) Manual hyperinflation the NICE guidance?
(e) Ventilator hyperinflation (a) 15 minutes
3. Which of these complications can occur due to bed rest (b) 25 minutes
within the critical care unit (choose all that apply)? (c) 30 minutes
(a) Muscle atrophy (d) 45 minutes
(b) Reduced joint range of movement (e) 60 minutes
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Section 4 Advanced Organ Support
Percutaneous Mechanical Circulatory

Chapter
21 Support
Evgeny Pavlushkov and Marius Berman
Short-term mechanical circulatory support (MCS) the inner lumen is open to the aorta and is used for
devices are used to maintain haemodynamic stability direct arterial pressure monitoring. Helium is less
in cardiogenic shock and provide reliable oxygenation soluble than some other gases (CO2) and it is also less
in acute cardiovascular and/ or respiratory failure. dense, which reduces travel time along the circuit and
Percutaneous MCS is used as a temporary meas- allows quick inflation and deflation of the balloon.
ure (bridge) to recovery of definitive management. IABP is usually positioned in the descending thoracic
These devices may be used in the following clinical aorta through one of the femoral arteries using the
situations: Seldinger technique.
• high-risk coronary or valve interventions The balloon inflates during diastole and displaces
(complex coronary anatomy, impaired LV the blood in the aorta, increasing diastolic and mean
function); pressure and thus augmenting coronary perfusion.
• cardiogenic shock complicating myocardial During systole, the balloon deflates, producing some
infarction; vacuum effect and therefore reducing the afterload for
• acute decompensated heart failure; the left ventricle (LV) and systolic pressure. This results
• bridge to heart transplantation; in improved emptying of the heart, and therefore
reduction of the wall stress of the heart. Other impor-
• bridge to recovery after allograft rejection;
tant haemodynamic effects of IABP include: reduction
• postcardiotomy cardiogenic shock;
of the heart rate (by 20%), decrease in the pulmonary
• acute cardiac, lung allograft failure;
capillary wedge pressure (by 20%) and rise in cardiac
• circulatory support before and after durable output (by 0.5 l/min or by 20%). The magnitude of the
LVAD implantation; effects can vary and depends on many factors: the vol-
• bridge to recovery after lung transplantation for ume of the IABP (bigger balloons, 50 cm3, displace more
pulmonary hypertension. volume, hence are more effective), its optimal position
The main objectives of temporary circulatory sup- (the tip of the IAB should be located 2 cm caudally to
port are to provide systemic perfusion and secondly the origin of the left subclavian artery which is easily
unload the heart to maximise chances of its recovery. confirmed by chest X-ray as 2 cm above the tracheal
Several types of percutaneous MCS options are bifurcation, or by TOE), optimal timing of the infla-
available for advanced heart/lung failure: intra-aortic tion/deflation cycle, heart rate and aortic compliance.
balloon pump (IABP), extracorporeal membrane oxy- The maximum haemodynamic effect from IABP
genation, Impella axial flow pump and TandemHeart counterpulsation is achieved when it is set to inflate
centrifugal pump. just after the aortic valve closure (dichrotic notch on
the arterial trace) and deflate just before aortic valve
IABP opening (upstroke part on the arterial waveform of
IABP is the most commonly used device for mechani- the next cardiac cycle). Early/late inflation as well as
cal circulatory support. It consists of two parts: the early/late deflation could lead to suboptimal diastolic
intra-
aortic balloon itself (IAB), a double lumen augmentation and reduced haemodynamic benefits of
catheter 7–8 French size; and a console containing the IABP (Figure 21.1).
the controller, pump and helium cylinder. The outer Timing of IABP is important as too early or too
lumen of the balloon is a gas containing chamber and late inflation or deflation can in fact worsen cardiac
14:41:15
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Section 4: Advanced Organ Support
R R
T T
P P
Q S Q
S
diastolic augmentation dichrotic notch
systolic unloading
IABP IABP
Figure 21.1 Aortic pressure waveform with IABP off and on. Inflation of the balloon corresponds to the augmented diastolic pressure. Note
the decrease of systolic pressure in assisted beat.
output and increase preload. Figure 21.2 illustrates achieved either by gradual (over hours) decrease of
some problems with timing of IABP. the ratio of augmented to non-augmented beats (from
1:1 to 1:2, 1:3 and so on), or by degree of inflation of
Alternative Routes for IABP Insertion the balloon, or a combination of both. According to
a recent survey, 57% of centres preferred to wean by
Transfemoral percutaneous method of insertion is a
reducing the ratio.
first choice option for IAB insertion. However, it can
Complications of IABP use include vascular lac-
be technically challenging or impossible in patients
eration or dissection, limb ischaemia, haemorrhage,
with significant peripheral vascular disease or previ-
balloon rupture, cholesterol embolisation, cerebro-
ous vascular operations on the iliofemoral segment
vascular events, haemolysis, thrombocytopenia,
or just small calibre arteries. Subclavian, axillary,
infection and peripheral neuropathy. The incidence
brachial arteries have been reported to be used to
of major complications should not exceed 2.6% and
access the thoracic aorta for IAB placement in dif-
IABP related mortality is only 0.5%.
ferent clinical settings. Direct access to the thoracic
Anticoagulation has traditionally been used
aorta can also be used as the entry site for the IABP.
with IABP to reduce thrombosis and embolisation.
This technique requires an open chest and is there-
However, existing data suggest that omitting heparin
fore used intraoperatively during cardiac operations
is safe in the context of IABP counterpulsation and
(Figure 21.3).
allows avoidance of bleeding related complications.
Common indications for IABP use have been
Duration and Weaning from the IABP refractory hypotension or haemodynamic instabil-
There is little evidence to guide the optimal duration ity of cardiac origin, mechanical complications of
and weaning strategy for IABP. Duration is mainly MI (MR, VSD), postcardiotomy shock, as a bridge
determined by patient need, institutional preferences to cardiac surgery/transplantation or as an adjunct
and individual clinical circumstances of the patients. in high- risk coronary interventions. However, the
Given the invasive nature of the device, the IABP data from large randomised trials and meta-analysis
should be removed as soon as the haemodynamic (IABP-SHOCK II) downgraded the impact of IABP
situation improves to the degree when the IABP is no in patients with acute MI complicated by cardio-
longer required or a more definitive treatment option genic shock undergoing revascularisation as it did not
becomes available. The weaning of the IABP can be reduce mortality. The routine use of IABP is no longer
14:41:15
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Chapter 21: Percutaneous Mechanical Circulatory Support
EARLY INFLATION AUG LATE INFLATION AUG

SYS
IAB is inflated SYS DN is visible ASYS
ASYS
well before between points
actual DN DN SYS/AUG DN
(aortic valve Violates
closure). Rule1
DIA
Violates Rule 1 DIA for inflation ADIA
for inflation ADIA
Result: Premature closure of aortic valve Result: AUG less than optimum
Reduces stroke volume/CO Decreased perfusion pressure
Increase in LVED volume and volume to coronary arteries
Increase in LV wall tension
EARLY DEFLATION LATE DEFLATION AUG

AUG SYS
ASYS = SYS ADIA > DIA
SYS ASYS ASYS
Violates Rule 3 Violates Rule 2
for deflation for deflation DN
DN
May see
“U” shape
at ADIA DIA
DIA ADIA
ADIA
Result: No afterload reduction Result: Increased workload of left ventricle
Increased MVO2
Figure 21.2 Timing problems with IABP. (A black and white version of this figure will appear in some formats. For the colour version, please
refer to the plate section.)
recommended by the European Society of Cardiology cava and expels it to the pulmonary artery, providing
(ESC) for this indication. flow above 4 l/min). Most of these modifications can be
inserted using a standard Seldinger technique. Impella
Impella (LV to Aorta) 5.0, although providing higher flows, requires surgical
The Impella (Abiomed, USA) is a temporary ventricu- cut-down to the artery due to its bigger size, making it
lar assist device designed for percutaneous insertion less convenient for insertion in an emergency setting.
through the femoral artery, which is advanced along Working in series with the LV (or RV in the case of
the aorta, across the aortic valve into the left ventricle Impella RP) the device unloads the ventricle, reduces
(Figure 21.4). It employs the principle of the Archimedes wall stress and oxygen demand, reduces ventricular
screw: blood enters the inflow at the tip of the catheter stroke work, and increases mean arterial pressure and
and is transported to the ascending aorta, generating cardiac output. Impella 2.5 is approved for use for up
non-pulsatile axial flow. Four versions of the pump are to 5 hours in the USA and up to 6 days in Europe.
currently available: Impella 2.5 (flow up to 2.5 l/min), Impella RP can provide temporary support for up to
Impella CP (3.0–4.0 l/min), Impella 5.0 (up to 5 l/min) 14 days. The safety and feasibility of Impella pumps
and Impella RP (designed for right ventricular (RV) as well as their positive impact on haemodynamics
support, this drains the blood from the inferior vena were demonstrated in trials involving different patient
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176
Figure 21.4 Diagram demonstrating the Impella LP2.5 axial

flow left ventricular assist device sitting across the aortic valve.
Reprinted with permission from Abiomed (Aachen, Germany),
the manufacturer of this device. (A black and white version of this
figure will appear in some formats. For the colour version, please
Figure 21.3 Transthoracic approach to IABP insertion. (A black
and white version of this figure will appear in some formats. For the
colour version, please refer to the plate section.)
this purpose, the inflow cannula is positioned into
the right atrium and blood is returned to the pulmo-
populations: acute myocardial infarction compli- nary artery. TandemHeart can generate flow of up to
cated by cardiogenic shock (ISAR-Shock), high-risk 5 l/min (with 19F arterial cannula). It is approved for
PCI (PROTECT II) and postcardiotomy cardiogenic circulatory support for up to 6 hours in the USA and
shock (RECOVER-I). However, the impact of these up to 30 days in Europe. Preserved RV function is
devices on mortality has yet to be established in larger essential for optimal performance of TandemHeart
randomised trials. as well as for Impella since both devices depend on
LV preload.
Similar to Impella, clinical data available sug-
TandemHeart (LA to Aorta) gest that TandemHeart increases blood pressure
TandemHeart (CardiacAssist, USA) is a percutane- and cardiac index, decreases pulmonary capillary
ously inserted device, which uses an extracorpor- pressure and improves perfusion of end organs;
eal centrifugal pump to transfer blood from the however, evidence of influence on mortality is lack-
left atrium to the aorta via the femoral artery in ing at present.
non-pulsatile fashion (Figure 21.5). In contrast to
Impella, TandemHeart requires two cannulas: the
inflow cannula inserted via the femoral vein and
Comparison of Percutaneous MCS
positioned into the left atrium through the intera- Devices
trial septum, and the second cannula in the femoral Each percutaneous device for short-term mechani-
artery. This configuration bypasses the left ventricle, cal circulatory support has unique characteristics and
offloads it and reduces LV workload. The circuit can haemodynamic profile. The choice of the particular
be reconfigured to support the right ventricle. For device should be guided by specific cardiovascular
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177
Figure 21.5 TandemHeart consists

of a 21F inflow cannula in the left
atrium after femoral venous access
and transseptal puncture and a 15F
to 17F arterial cannula in the iliac
artery. Reproduced with permission
from Naidu (2011). (A black and white
version of this figure will appear in
some formats. For the colour version,
goals and clinical context of the individual patient • The choice of the particular device should be
(Table 21.1). guided by specific cardiovascular and respiratory
Most of the current knowledge and guidelines goals, and clinical context of an individual patient
for percutaneous mechanical circulatory support are as well as expertise available.
based on observational data, expert opinion, retro-
spective studies and consensus agreement. More pro-
spective randomised studies are needed to establish Further Reading
evidence-based background for this fast evolving field Bignami E, Tritapepe L, Pasin L, et al. A survey on the use
of cardiothoracic medicine. of intra-aortic balloon pump in cardiac surgery. Annals
of Cardiac Anaesthesia. 2012; 15: 274–277.
Cheng JM, den Uil CA, Hoeks SE, et al. Percutaneous left
Learning Points ventricular assist devices vs. intra-aortic balloon pump
counterpulsation for treatment of cardiogenic shock: a
• There are two main objectives of temporary
meta-analysis of controlled trials. European Heart
circulatory support: (1) to provide perfusion for Journal. 2009; 30: 2102–2108.
end organs and (2) to unload the heart to maximise
Ferguson JJ, Cohen M, Freedman RJ, et al. The
chances of its recovery or bridge for further therapy.
current practice of intra-aortic balloon
• Each percutaneous device for short-term counterpulsation: results from the Benchmark
mechanical circulatory support has unique Registry. Journal of the American College of Cardiology.
characteristics and haemodynamic profile. 2001; 38: 1456–1462.
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Table 21.1 Comparison of percutaneous MCS devices
IABP ECMO TandemHeart Impella 2.5 Impela 5.0 Impella RP

Pump Pneumatic Centrifugal Centrifugal Axial flow Axial flow Axial flow
mechanism
Cannula size 7–9F 18–21F inflow, 21F inflow, 15–17F 13F 22F 22F
15–22F outflow outflow
Insertion Descending Inflow cannula 21F inflow 12F catheter 21F catheter Via the femoral
technique aorta via into RA via cannula into LA placed placed vein, into the
femoral artery, femoral vein, via femoral vein retrogradely retrogradely right atrium,
Seldinger outflow cannula and transseptal across aortic across aortic across the
technique into descending puncture and valve via valve via surgical tricuspid and
aorta via femoral 15–17F outflow femoral artery cutdown of pulmonic
artery cannula into femoral artery valves, and into
femoral artery the pulmonary
artery
Haemodynamic 0.5 l/min >4.5 l/min 4 l/min 2.5 l/min 5.0 l/min >4 l/min
support
Implantation + ++ ++++ ++ ++++ ++
time
Risk of limb + +++ +++ ++ ++ +
ischaemia
Anticoagulation + +++ +++ + + +
Haemolysis + ++ ++ ++ ++ ++
Management + +++ ++++ ++ ++ ++
complexity
Modified from Ouweneel and Henriques (2012).
Kogan A, Preisman S, Sternik L, et al. Heparin-free co-operative clinical trial. New England Journal of
management of intra-aortic balloon pump after cardiac Medicine. 1973; 288: 979–984.
surgery. Journal of Cardiac Surgery. 2012; 27: 434–437.
Thiele H, Sick P, Boudriot E, et al. Randomized comparison
Naido SS. Contemporary reviews in cardiovascular of intra-aortic balloon support with a percutaneous left
medicine, novel percutaneous cardiac assist devices: ventricular assist device in patients with revascularized
the science of and indications for hemodynamic acute myocardial infarction complicated by
support. Circulation. 2011; 123: 533–543. cardiogenic shock. European Heart Journal. 2005;
Ouweneel DM, Henriques JPS. Percutaneous cardiac 26: 1276–1283.
support devices for cardiogenic shock: current Thiele H, Zeymer U, Neumann F-J, et al. Intra-aortic
indications and recommendations. Heart. 2012; balloon counterpulsation in acute myocardial
98: 1246–1254. infarction complicated by cardiogenic shock
Pucher PH, Cummings IG, Shipolini AR, McCormack DJ. (IABP-SHOCK II): final 12 month results of
Is heparin needed for patients with an intra-aortic a randomised, open-label trial. Lancet. 2013;
balloon pump? Interactive Cardiovascular and Thoracic 382: 1638–1645.
Surgery. 2012; 15: 136–139. Unverzagt S, Buerke M, de Waha A, et al. Intra-aortic
Rihal CS, Naidu SS, Givertz MM, et al. SCAI/ACC/HFSA/ balloon pump counterpulsation (IABP) for
STS Clinical Expert Consensus Statement on the use of myocardial infarction complicated by cardiogenic
percutaneous mechanical circulatory support devices shock. Cochrane Database of Systematic Reviews. 2015;
in cardiovascular care. Journal of the American College 3: CD007398.
of Cardiology. 2015; 65: e7–26. Windecker S, Kolh P, Alfonso F, et al. 2014 ESC/EACTS
Scheidt S, Wilner G, Mueller H, et al. Intra-aortic balloon guidelines on myocardial revascularization. Revista
counterpulsation in cardiogenic shock. Report of a Española de Cardiología (English Edition). 2015; 68: 144.
14:41:15
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MCQs
1. What are the advantages of using helium in IABP? (c) Decrease diastolic BP
(a) High solubility (d) Has no effect on heart rate
(b) Availability (e) Increase pulmonary capillary wedge pressure
(c) Low density 4. The least common complication of IABP is:
(d) High biocompatibility (a) Peripheral neuropathy
(e) Lack of thrombogenicity (b) Bleeding
2. What is the optimal position of the IAB tip on (c) Limb ischaemia
chest X-ray? (d) Infection
(a) 2 cm below bifurcation of the carina (e) Thrombocytopenia
(b) 1 cm cranial to the origin of the left 5. All statements regarding TandemHeart are true except
subclavian artery one:
(c) Highest point of the aortic arch (a) Requires interatrial septum puncture
(d) 2 cm cephalad to bifurcation of the trachea (b) Reduces pulmonary capillary wedge pressure
(e) At the level of angle of Louis (c) Improves organ perfusion
3. Which of the following is a haemodynamic effect (d) Was demonstrated to reduce mortality
of IABP?
(e) Is licensed for use for up to 30 days in Europe
(a) Decrease systolic BP
(b) Has no effect on mean BP
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Ventricular Assist Devices (VAD)

Chapter
22 Harikrishna M Doshi and Steven SL Tsui
Introduction it to the pulmonary artery. VADs provide life support

for patients with failing ventricle(s) by maintaining
The UK National Heart Failure Audit 2013–2014 esti-
perfusion to vital organs. The basic components of a
mated that there are 2 million people in the UK suffer-
VAD system are as follows.
ing from heart failure, a figure that is likely to rise due
to improved survival following heart attack and more 1. Inflow cannula –for draining blood from the
effective treatment. Heart transplant has remained a patient to the blood pump.
therapeutic cornerstone for patients with end stage 2. Blood pump –usually consists of a motor and an
heart failure when optimum medical therapy has impeller for driving the blood.
failed. It offers an excellent short and long term out- 3. Outflow cannula –returns blood from the pump
come with median survival of 11 years. Major limita- to the patient.
tion in expansion of heart transplantation is the limited 4. Driveline –a composite cable for the transfer of
availability of donor organs. According to the 2015 electrical signal and power between the blood
Annual Report on Cardiothoracic Transplantation in pump and the console.
the UK, only 30% of non-urgent heart patients were 5. Controller –controls blood pump operation and
transplanted within 6 months of their listing, during displays pump performance parameters.
which time 9% died awaiting a transplant. 6. Rechargeable battery pack –to power the motor of
Exciting new developments are being trialled to the blood pump.
increase the donor pool, for example transplanting
heart from donation after circulatory death. However,
donor heart numbers will never satisfy the rapidly Temporary MCSD
expanding cohort of patients who require cardiac
replacement therapy. Many such patients are over Indications
75 years of age and with comorbidities which make For patients who require mechanical circulatory sup-
them unsuitable for heart transplant. Besides, many port (MCS) over days to weeks, temporary devices
patients on the list deteriorate and cannot survive the may be used as a bridge to recovery, bridge to trans-
wait for a transplant without other intervention. In plant or bridge to a longer term device, i.e. bridge to
1978, Dr Denton Cooley reported the first successful bridge. Temporary MCS (Table 22.1) may be indicated
bridging to transplant using mechanical heart sup- in patients with decompensated heart failure, acute
port, and since then rapid strides have been made in cardiogenic shock or arrested patients with uncertain
the field of mechanical circulatory support devices neurology, to assess recovery of end organ function
(MCSD). before deciding on the next step (bridge to decision).
Ventricular assist devices (VAD) are mechanical They may also be considered for patients with severe
blood pumps that work in parallel or in series with the symptomatic acute heart failure where myocardial
native ventricle(s). Most commonly, a left ventricular recovery is anticipated, for example fulminant myo-
assist device (LVAD) draws oxygenated blood from carditis. Occasionally it may be indicated in post-
the left atrium or ventricle and returns it to the aorta; cardiotomy cardiogenic shock where weaning from
a right ventricular assist device (RVAD) draws venous cardiopulmonary bypass fails. The aim is to provide
blood from the right atrium or ventricle and returns short term support while other medical problems such
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Chapter 22: Ventricular Assist Devices (VAD)
Table 22.1 Indications of temporary MCSD uses a priming volume of 31 ml. The CentriMag sys-
• Cardiogenic shock due to acute myocardial infarction tem can be used to provide left or right ventricular
• Postcardiotomy shock support and it can also be used in an ECMO circuit.
• High risk percutaneous coronary intervention, ventricular The CentriMag system is most commonly implanted
tachycardia ablation through a sternotomy incision in the operating room.
• Acute rejection post cardiac transplant with haemodynamic Anchoring of the percutaneous vascular cannulae
compromise
as they traverse the anterior abdominal wall allows
• Bridge to LVAD or transplant
the patient limited mobilisation and rehabilitation.
• Right ventricular failure
Bedside pump changes can be performed in awake
patients every 30 days, allowing patients to be sup-
ported for months on the CentriMag system.
as infection, renal failure and neurological assessment
can be dealt with and prognosis of the patient can be
better defined. Implantable or Durable VAD
Implantable VAD are designed to provide durable
Types of Temporary Mechanical Circulatory circulatory support for patients with advanced heart
faiure. Patients can be supported with these devices
Support for months or years. The main advantage of durable
1. Extracorporeal life support (ECLS) or cardiac VAD is to allow implanted patients to return to the
ECMO (see Chapter 23): community and lead an active life. Currently, LVAD is
(a) Peripheral cannulation; the most common type of durable MCSD implanted.
(b) Central cannulation.
2. Percutaneous devices: Types of Long Term VAD
(a) Intra-aortic balloon pump (IABP) (see • First generation LVADs such as the Thoratec
Chapter 21); HeartMate XVE, PVAD and IVAD were pulsatile
(b) Impella devices: 2.5, CP, 5.0, LD devices. They consisted of a pump housing with
(Abiomed Inc., MA, USA), transaortic a diaphragm and unidirectional valves to pump
intraventricular pump; blood in a pulsatile manner, typically ejecting 80
(c) TandemHeart System (CardiacAssist, Inc., PA, to 100 times per minute. In 2001, results of the
USA), transvenous transseptal left atrium to REMATCH study showed that patients with end
arterial pump. stage heart failure not eligible for transplantation
3. Non-percutaneous devices: for example who were implanted with the HeartMate VE
CentriMag centrifugal pump (Thoratec had a significant survival advantage at 1 year
Corporation, CA, USA). compared with patients who were managed
with optimal medical therapy. However, first
Characteristics of Impella devices are given in
generation LVAD were bulky, less durable and
Table 22.2, and contraindications to temporary
had high complication rates including bleeding,
MCSD are listed in Table 22.3.
infection, stroke, device malfunction and
development of right heart failure. Over the last
Non-percutaneous Devices: CentriMag 10 years, outcomes with continuous flow devices
The CentriMag (Thoratec Corporation, CA, USA) sys- have been shown to be far superior to outcomes
tem is an extracorporeal circulatory support device. with pulsatile devices. As a result, first generation
It has a disposable polycarbonate pump (Figure 22.1) LVADs have become obsolete.
mounted on a reusable motor. The magnetically levi- • Second generation VAD are axial flow pumps
tated pump impeller provides a friction-free blood with a single moving impeller mounted on
path which minimises blood trauma and haemolysis. mechanical bearings spinning at high speed. They
It is approved for use for up to 30 days and has been are smaller in size and more durable than their
widely adopted with reasonable success. This device predecessors. These devices are silent in operation
can produce flows of up to 9.9 l min−1 in vitro and and provide continuous blood flow with reduced
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Figure 22.1 CentriMag primary console and centrifugal pump (courtesy of Thoratec Corporation, CA, USA). (A black and white version of
this figure will appear in some formats. For the colour version, please refer to the plate section.)
Table 22.2 Types of Impella devices and characteristics
Device and function Impella 2.5 Impella CP Impella 5/LD Impella RP

Access Percutaneous Percutaneous Surgical, axillary, femoral or Percutaneous
femoral femoral ascending aorta femoral vein
Maximum output, litre per 2.5 4.0 5.0 4.6
minute
Catheter size, F 9 9 9 11
Motor size, F 12 14 21 22
Maximum revolutions per 51,000 46,000 33,000 33,000
minute (rpm)
EU approved duration of use, 5 5 10 14
days
pulsatility. They include devices like the

Thoratec HeartMate II and Jarvik 2000
Indications and Patient Selection
Current indications for LVAD therapy can be broadly
amongst others.
classified as follows.
• Third generation pumps use hydrodynamic
and/or electromagnetic bearings to suspend 1. Bridge to transplant (BTT): For patients eligible
the impeller inside the pump housing, thereby for heart transplant but deteriorating before a
eliminating contact between moving parts and donor heart is available.
avoiding friction. Their smaller size allows 2. Bridge to candidacy (BTC): For patients with
intrathoracic placement (Figure 22.2) and contraindication(s) to heart transplantation
obviates the need for an abdominal pump secondary to advanced heart failure, such as renal
pocket. Examples of third generation devices dysfunction or pulmonary hypertension, that
include the HeartWare HVAD and the Thoratec is potentially reversible after a period of LVAD
HeartMate 3. support.
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Table 22.3 Contraindications and complications associated with temporary circulatory support
Device Contraindications Complications

All devices Severe peripheral vascular disease Bleeding
Irreversible neurological disease Vascular injury
Sepsis Infection
Neurological injury
Impella LV thrombus Haemolysis
Moderate to severe aortic stenosis Pump migration
Moderate to severe aortic insufficiency Aortic valve injury
Mechanical aortic valve Aortic insufficiency
Recent TIA or stroke Tamponade due to LV perforation
Aortic abnormalities Ventricular arrhythmia
Contraindication to anticoagulation
TandemHeart Ventricular septal defect Cannula migration
Moderate to severe aortic insufficiency Tamponade due to perforation
Contraindication to anticoagulation Thromboembolism
Air embolism during cannula insertion
Interatrial shunt development
CentriMag Contraindication to anticoagulation Thromboembolic events
Air embolism
Figure 22.2 (a) HeartMate 3 with its controller. (b) HeartWare HVAD with driveline. (c) Diagram of a patient with a HeartWare HVAD sited
in the left ventricular apex and a percutaneous driveline going to a wearable controller and batteries. (Courtesy of Thoratec Corporation,
CA, USA and HeartWare Corporation, MA, USA). (A black and white version of this figure will appear in some formats. For the colour version,
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Table 22.4 INTERMACS profile descriptions
INTERMACS level Definition Description

1: Critical Crash and burn Haemodynamic instability in spite of increasing doses of catecholamines and/or
cardiogenic shock mechanical circulatory support with critical hypoperfusion of target organs (severe
cardiogenic shock)
2: Progressive Sliding on inotropes Intravenous inotropic support with acceptable blood pressure but rapid deterioration
decline of kidney function, nutritional state, or signs of congestion
3: Stable but Dependent stability Patient with stable blood pressure, organ function, nutrition and symptoms on
inotrope dependent continuous intravenous inotropic support (or a temporary circulatory support device
or both), but demonstrating repeated failure to wean from support due to recurrent
symptomatic hypotension or renal dysfunction
4: Resting symptoms Frequent fliers Patient can be stabilised close to normal volume status but experiences daily
symptoms of congestion at rest or during activities of daily living (ADL); doses of
diuretics generally fluctuate at very high levels
5: Exertion intolerant Housebound Complete cessation of physical activity, stable at rest, but frequently with moderate
water retention and some level of kidney dysfunction
6: Exertion limited Walking wounded Minor limitation on physical activity and absence of congestion while at rest; easily
fatigued by light activity
7: Advanced Placeholder Patient in NYHA functional class II or III with no current or recent unstable fluid balance
NYHA III
3. Destination therapy (DT): As a permanent retrospective studies on patients supported with pul-
treatment for patients who are not eligible for satile devices. A validation study on continuous-flow
heart transplant. LVAD recipients showed that none of the described
The Interagency Registry for Mechanically Assisted risk models reliably predicted the need for RVAD sup-
Circulatory Support (INTERMACS) is a North port post LVAD. In any case, preoperative risk models
American registry established in 2005 to collect clini- would not be able to take account of intraoperative
cal data on patients receiving mechanical circulatory events.
support. The INTERMACS stratifies patients with
Echocardiographic Assessment
advanced heart failure into seven profiles based on
their clinical status as outlined in Table 22.4. Numerous echocardiographic parameters for assess-
ing RV function have been described and some
are listed below. However, their usefulness in
Risk Factors and Their Assessment for predicting RV failure after LVAD implant are still
Implantation for VAD debated.
• Visual assessment: volumetric assessment of RV
Cardiac Factors function is challenging and many physicians rely
Right ventricular (RV) function is one of the most on visual assessment to estimate RV size and
important parameters to consider before LVAD function.
implantation. Adequacy of RV function after LVAD • Tricuspid annular plane systolic excursion
implantation is a balance between the intrinsic RV (TAPSE): assess RV systolic longitudinal function
function and the RV afterload. During RV ejection, of RV. TAPSE < 16 mm indicates RV systolic
RV afterload is proportionate to pulmonary artery dysfunction. TAPSE correlates well with RV
pressure, which is a sum of the impedance of the pul- global systolic function.
monary vasculature and the left atrial pressure. • Right ventricular index of myocardial
A number of risk prediction models for RV fail- performance (RIMP): RIMP > 0.40 by pulse
ure following LVAD insertion have been described. Doppler indicates RV dysfunction; fractional area
However, these have all been derived from change (FAC) <35% indicates dysfunction.
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• RV diastolic function can be assessed by tricuspid

inflow velocities, pulsed Doppler imaging of
Non-cardiac Factors
Presence of end organ dysfunction is a risk factor for
hepatic veins and measurement of IVC size and
poor outcome. Contraindication to LVAD implanta-
collapsibility. Tricuspid E/A ratio <0.8 indicates
tion includes the following:
impaired relaxation.
• Tricuspid valve regurgitation (TR) can help • Irreversible end organ failure, especially renal,
assessment of right atrial pressure in the absence of hepatic and respiratory system. Parameters such
right ventricular outflow obstruction (RVOT). TR as elevated bilirubin, elevated prothrombin time
velocity >2.8 to 2.9 m/second corresponds to systolic suggest an auto-anticoagulated state signifying
pulmonary artery pressure (PAP) of approximately reduced hepatic synthetic function and may be
36 mmHg assuming right atrial pressure (RAP) of signs of underlying right heart dysfunction.
3–5 mmHg, and indicates elevated RV systolic and • Active and uncontrolled systemic infection.
pulmonary artery pressures. • Irreversible neurological injury. Recent stroke will
increase risk of bleeding.
Invasive Monitoring • Contraindication to systemic anticoagulation or
Transpulmonary gradient (TPG) is the difference antiplatelet therapy.
between mean pulmonary artery pressure and left • History of substance abuse or non-compliance.
atrial pressure (estimated by pulmonary capillary
wedge pressure (PCWP)). Assessment of the TPG is Perioperative Management of Patients
recommended for the detection of pulmonary vas-
cular disease in left heart conditions associated with Undergoing VAD Implantation
elevated pulmonary venous pressure. Elevated pulmo-
nary vascular resistance (PVR) is present when PVR is
Preoperative Preparations
≥ 3 Wood units or TPG ≥ 12 mmHg. The assessment of patients for LVAD therapy con-
The optimal haemodynamic parameters of pre- sists of detailed medical, physical and psychosocial
operative RV function indicating a low likelihood of assessment. Cardiovascular investigations including
developing RV failure include: echocardiogram and right heart catheterisation are
essential to assess right heart function. CT scan of
• CVP ≤8 mmHg
the thorax may help identify underlying pulmonary
• PCWP <18 mmHg
disease and establishes the anatomy of the LV apex.
• CVP/PCWP ≤0.66
Other investigations to assess kidney, liver and lung
• PVR ≤2 Wood units function are essential. Abnormal results will require
• RVSWI ≥400 l min-2 m-2. further evaluation and efforts to optimise end organ
Right ventricular stroke work index (RVSWI) = CI/ functions must be undertaken. Active malignancy
HR × 1000 × (mPAP –RAP), where CI is cardiac should be ruled out. Infection screen is essential
index in l m−2; HR is heart rate in beats per minute; to rule out any existing infection, hepatitis or HIV.
mPAP is mean pulmonary artery pressure in mmHg; Dental checks should be carried out prior to surgery.
RAP is right atrial pressure in mmHg. Psychosocial assessment is very important. Patients
Other intracardiac lesions such as aortic valve will need robust social support and a thorough under-
regurgitation or patent foramen ovale (PFO) will standing of possible complications.
need to be corrected because after LVAD implanta- It is important to educate the patient and their fam-
tion, decompression of the left heart will increase the ilies about risks and benefits of LVAD therapy. The
amount of aortic valve regurgitation and allow right patient’s understanding and expectations are impor-
to left shunt across a PFO, leading to significant oxy- tant considerations before accepting the patient for
gen desaturation. It will also increase the chance of long term LVAD therapy. In complex situations, psy-
paradoxical embolisation. Intracardiac repairs have chiatric evaluation may be pivotal in decision making.
an impact on the conduct of surgery since use of car- Extensive teaching and training through multidisci-
diopulmonary bypass will be required with or without plinary support staff is an integral part in preparing
a period of myocardial ischaemia. patients for LVAD implantation.
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Table 22.5 Essential components of VAD care surgeons, intensivists, physiotherapists, nutritionists,

• Exercise and physical therapy microbiologists, pharmacists and psychiatrists. VAD
• Nutrition coordinators are central in organising various activi-
• VAD self-care ties for these patients. They remain a constant point
• Driveline site dressing changes of contact in maintaining continuity of care when
• System controller checks patients have been discharged into the community.
• VAD log book VAD coordinators are usually specialist nurses or
• Activity restrictions physician assistants with an in depth knowledge of all
aspects of LVAD care, equipment and support. Once
the decision to implant a durable LVAD is made, they
Care in the ITU, Ward and Discharge are actively involved in education and training of the
patient and family. They also work with other team
Planning members and arrange activities with patient and fam-
Durable LVAD implantations are generally carried out ily in such a way that they are ready for self-care by the
using a median sternotomy incision and cardiopul- time of discharge. Following discharge, they help tran-
monary bypass. Some units adopt a minimally inva- sition home visits to community nurses but remain a
sive approach using ministernotomy and small left point of contact for the patient and their family for
anterior thoracotomy. Careful consideration is neces- support or advice.
sary whilst dressing and securing the drive line exit Chronic heart failure can lead to malnutrition and
site right from theatre. wasting which may have a negative impact on wound
The early phase of patient return into the ITU healing and immune resistance. The dietician moni-
requires careful monitoring and optimisation of pump tors caloric intake and makes recommendations on
speed, flows, filling status and attention to tissue per- nutritional supplements. Physiotherapists help with
fusion status using various parameters such as mixed early mobilisation and restore patient confidence and
venous oxygen saturation. Any coagulopathy should independence.
be corrected to avoid bleeding. A pulmonary artery There are some issues unique to the clinical man-
catheter is a valuable tool to assist with haemodynamic agement of LVAD supported patients.
monitoring. Acidosis, hypoxia and hypercapnoea can
potentially result in pulmonary vasoconstriction and • Measurement of blood pressure: Due to the
therefore should be avoided. If inhaled nitric oxide continuous flow nature of modern LVADs,
was required during the implant procedure, early Korotkoff sounds cannot be heard with a
weaning may be facilitated by the use of nebulised ilo- stethoscope while measuring blood pressure. For
prost at intervals. The latter could be transitioned to the same reason, non-invasive blood pressure
oral sildenafil after extubation if required. measurement devices are ineffective. A Doppler
After a period of stability has been achieved, early probe and a sphygmomanometer must be used to
return to spontaneous respiration and extubation measure average blood pressure.
allows for early mobilisation and minimises the period • High blood pressure: Hypertension is commonly
on mechanical ventilation. Careful fluid balance mon- observed after implantable LVAD therapy. This
itoring and aggressive use of diuretic therapy helps will have a negative impact on pump flow since
optimise intravascular volume status. Renal, liver and LVAD output is preload dependent and afterload
other end organ function must be regularly assessed sensitive. Hypertension has also been shown to be
to make sure that they are recovering with improved associated with an increased risk of intracranial
end organ perfusion. The key issues are early mobi- haemorrhage in LVAD supported patients.
lisation, good nutrition and meticulous wound care Therefore, careful control of blood pressure with
(see Table 22.5). vasodilator therapy is essential.
• Anticoagulation: Due to the contact of blood
The VAD Team component to artificial surfaces, anticoagulation
Care of the patient with durable VAD necessitates a is necessary. Current International Society
team approach (Figure 22.3). The VAD team consists for Heart and Lung Transplantation (ISHLT)
of a multitude of specialties including cardiologists, recommendation is to prescribe both antiplatelet
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Cardiologist Cardiac Surgeon
Patient and
Family
Psychiatrist Dietician
VAD Co-ordinator
Physiotherapist Pharmacist
Figure 22.3 Configuration of multispecialty VAD team.
therapy and warfarin to maintain device

specific INR.
Postimplant Adverse Events
• Arrhythmia and issues with ICD devices: One Bleeding
of the issues with excessive pump speed may be Early postoperative bleeding remains common after
suction causing collapse of the LV cavity and LVAD implantation. Immediately post implant,
ventricular arrhythmias. For patients who already the patient may be coagulopathic due to preop-
have a pacemaker or automatic implantable erative hepatic congestion or antiplatelet therapy.
cardioverter defibrillator (AICD) implanted A low threshold for re-exploration is required since
preoperatively, the device may need to be checked tamponade is poorly tolerated in these patients.
for compatibility and may need readjustment to Haemodynamic instability, rising filling pressures and
prevent unnecessary pacing or shocks. unexplained alterations in LVAD flows should raise
suspicion of tamponade. Causes of such postopera-
VAD Self-Care tive haemorrhage can be bleeding from anastomotic
In addition to medical and physical fitness, discharge sites, leaky connections or generalised coagulopathy.
planning requires complete independence for VAD Later onset bleeding may be caused by anticoagula-
self-care. The main elements for self-care are: tion therapy in combination with development of
• Once at home, patient and carer should be able acquired von Willebrand factor deficiency. Late bleed-
to take care of the equipment and ensure regular ing may occur from mucosal surfaces, especially from
cleaning. the gastrointestinal tract through arteriovenous mal-
formations. The HeartMate II destination therapy trial
• Drive line dressing needs meticulous attention
showed rates of bleeding requiring transfusion at 1.66
to aseptic techniques since exit site infection
and 1.13 events per patient year in early and mid trial
remains one of the commonest complications
groups.
and once established are very difficult to
eradicate.
• Regular record of vital signs and LVAD Right Heart Failure
parameters is essential. LVAD causes geometric changes to the right ventricle
• Shower is allowed with care of the console and and impairs global RV contractility with leftward sep-
batteries but bathing and swimming is not tal shift. The RV performance following LVAD implan-
permitted. Similarly, contact sports and strenuous tation depends on many factors including afterload,
activities are discouraged due to fear of device preload, ventriculoarterial coupling and ventricular
damage or drive line trauma. interdependence. The INTERMACS registry defines
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the right ventricular failure based on the following oxide (up to 5 ppm) and nebulised iloprost (2.5–
diagnostic criteria: 10.0 µg every 3 hours) or RVAD support.
• Symptoms and signs of persistent right
ventricular dysfunction. Infection
• Central venous pressure (CVP) >18 mmHg with a Sepsis occurs in 11– 26% of LVAD patients and
cardiac index (CI) < 2.0 l min−1 m−2 in the absence accounts for 21–25% of LVAD deaths. The commonest
of elevated pulmonary capillary wedge pressure area for infection is at the driveline exit site. The fifth
>18 mmHg, tamponade, ventricular arrhythmias annual report of INTERMACS reported a driveline
or pneumothorax. infection rate of 8 per 100 patient months. Infections
• Requiring RVAD implantation, or requiring of device pocket, blood and endocarditis are some of
inhaled nitric oxide or inotropic therapy for the other complications. Left pleural collection and
duration of more than 1 week at any time after formation of empyema is a possible complication for
LVAD implantation. a thoracotomy approach to implantation. High index
of suspicion, prompt treatment and active involve-
The severity of right heart failure has been classi-
ment of the microbiology team in the day to day
fied based on the following criteria:
management of these patients yields better long term
Severe: Need for RVAD. outcome. ISHLT has published guidelines for identifi-
Moderate: Need for inotrope or intravenous or cation of specific MCSD related infections.
inhaled pulmonary vasodilator (e.g.
prostaglandin E or inhaled nitric oxide).
Mild: Meeting two of the four clinical criteria
Thrombosis
listed below: Patients with LVAD are at risk of pump thrombosis
and other thromboembolic events. Pump thrombosis
• CVP > 18 mmHg or mean RA
can lead to pump obstruction, which can be fatal. It
pressure >18 mmHg;
results from ingestion of debris into the LVAD or in
• CI < 2.3 l min−1 m−2;
situ thrombosis and can occur as an early or late com-
• Ascites or evidence of moderate to plication. Risk factors for pump thrombosis include
worse peripheral oedema; inadequate anticoagulation, atrial fibrillation, hyper-
• Evidence of elevated CVP by echo coagulable state and coexistent infection. For continu-
(dilated inferior vena cava without ous flow LVAD, the rate of pump thrombosis ranges
collapse); from 0.01 to 0.11 per patient year. Patients may pre-
• physical exam (signs of increased sent with manifestations of heart failure and evidence
jugular venous pressure). of haemolysis in the form of red or reddish brown
In the HeartMate II destination therapy trial, 20% urine, worsening renal function, increased serum
of patients received extended inotropic therapy for LDH level and/or increased free plasma haemoglobin.
persistent heart failure and 4% required placement The LVAD power consumption is abnormally high
of RVAD. In the HeartWare ADVANCE BTT trial, with either power spikes or gradual increase in power
25% of patients were dependent on prolonged ino- requirement. Treatment of pump thrombosis includes
tropes and 3% required RVAD. The 1-year mortality augmentation of anticoagulation, thrombolytic ther-
rate for patients requiring RVAD support following apy and pump exchange.
LVAD implantation increases significantly from 21%
to 44%.
RV failure can be managed as follows:
Neurological Complications
Neurological complication remains a leading cause
• Preventive strategies include minimising fluid of long term morbidity and mortality. Stroke in
load, early extubation, maintaining sinus rhythm LVAD patients predominantly occurs in the right
and high index of suspicion. hemisphere. The fifth annual report of INTERMACS
• Management strategies include inotropes, reports a stroke risk of 11% at 1 year and 17% at
pulmonary vasodilators such as inhaled nitric 2 years. The mechanism of stroke may be partial
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cannula obstruction, deformation of blood pathway fifth annual report of INTERMACS reported 1, 2,
within the pump, twisting or kinking of outflow graft, 3 and 4 years survival at 80%, 70%, 59% and 47%
inadequate anticoagulation and infection. respectively.
Aortic Regurgitation Quality of Life and Functional Status

De novo aortic regurgitation has been observed in up One of the main objectives of LVAD therapy is to
to 25% of patients supported by continuous flow LVAD improve quality of life and functional status of patients
therapy. This complication is more commonly seen in with symptomatic heart failure. In the HeartMate II
patients in whom the aortic valve does not open dur- BTT and DT trials, approximately 80% of patients
ing LVAD support. Regurgitant aortic flow reduces reported improvement in their functional status from
the overall effectiveness of LVAD support and leads NYHA class IIIb to IV at baseline to class I or II.
to volume load of the left ventricle. Asymptomatic Between January 2007 and December 2013, there
patients can be treated by optimisation of pump flow have been 10 industry funded trials and registries, 10
under echo guidance to allow intermittent aortic multicentre reports and multiple single centre obser-
valve opening. Symptomatic patients will need higher vational experience. Using data from these studies, a
pump flows in the initial phases and in late phases single page pictogram (Figure 22.4) has been devel-
may require surgical intervention to replace the aortic oped which provides patients, their families and cli-
valve with a bioprosthesis or urgent transplant. nicians a visual representation of the full spectrum
of possible outcomes with LVAD therapy at 1 year.
Device Failure This serves as a useful tool to explain what could be
expected with LVAD therapy and help guide the deci-
This is generally a late complication. Failed external
sion making process.
components can generally be replaced and hence may
not be life threatening. Internal component failure
is uncommon these days except for pump thrombo- Future Directions
sis. Third generation continuous flow LVAD pumps Third generation continuous flow LVADs have already
use magnetic levitation impellers, which do not have paved the way for smaller devices that do not require
mechanical wear and are expected to be more durable an abdominal pump pocket. This allows LVAD
than the earlier generation devices. implantation through less invasive approaches and
Other complications include ventricular arrhyth- obviates the need for full sternotomy incision or even
mias, abdominal complications like device erosions or the use of CPB. This may reduce some of the common
adhesions and haemolysis. early postimplant complications such as bleeding and
right ventricular failure.
Outcomes Driveline exit site infection remains the Achilles’
heel of long term LVAD therapy at present. Device
For patients with advanced heart failure, outcome with
manufacturers have been developing fully implant-
medical therapy is dismal. LVAD support provides
able LVAD systems with internal batteries that could
marked improvement in quality of life, functional sta-
be recharged wirelessly. Such transcutaneous energy
tus and survival. Outcomes following treatment with
transfer systems (TETS) have already been tested in
continuous flow LVAD have continued to improve
small clinical trials as a proof of concept and have
over the last decade. However, despite improvements
shown promise.
in survival and symptoms of heart failure, LVAD ther-
With increasing experience of LVAD, it has
apy is still associated with a significant risk of major
become apparent that chronic low arterial pulsatil-
adverse events.
ity may contribute to complications such as arterio-
venous malformations and aortic valve insufficiency.
Survival Pump speed modulation that allows for greater pulsa-
The HeartWare ADVANCE BTT trial reported a tility is a focus of much research. Similarly, miniaturi-
1-year survival of 86%. The HeartMate II DT trial sation and remote monitoring are the other areas of
reported an actuarial survival of 58% at 2 years. The active development.
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190
Survival
80%
Benefits
1 year
Quality of Life*
0 Before LVAD = 28 1 year after LVAD = 70 100

Worst Best
Rehospitalised for Any Cause
55%
Major Bleeding†
0–1 months after LVAD (typically surgical) 1–12 months after LVAD
30% 20%
Stroke‡
10%
Risks
1 year
Serious Device-Related Infection§
20%
Device Malfunction Due to Clotting
5%
Ongoing Heart Failure
18%
Figure 22.4 1 year outcomes using weighted averages from LVAD studies (combined BTT and DT therapies). Shaded area, affected; white
areas, not affected. Quality of Life: Kansas City cardiomyopathy questionnaire score. Major bleeding: requiring transfusion or urgent medical
attention. Stroke: ischaemic 5% ± 5, haemorrhagic 5% ±4. Serious device related infection: driveline 18% ± 2, pump pocket 2% ± 2. Device
malfunction due to clotting: typically requiring surgery to replace the device. On-going heart failure: requiring inotropes >2 weeks after
implant 15% ± 7, requiring right ventricular assist device 3% ± 2.
LVAD therapy is a rapidly evolving branch of • However, with a rising incidence of heart failure
medicine. As the demand for donor hearts con- and shortages of donor hearts, it is inevitable that
tinues to outstrip the limited supply, we shall have more patients will require MCSD as a substitute.
to increasingly rely on the development of devices • The experience of managing MCS has grown
with better durability and reduced long term considerably leading to better patient selection
complications. and improved outcomes.
• For patients ineligible for transplantation,
Learning Points implantable LVAD can serve as an alternative
• Heart transplantation remains the best treatment treatment or destination therapy.
option for advanced heart failure patients with • Development of newer devices that enable less
median survival of 11 years post transplant. invasive implantation with lower adverse event
14:42:08
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rates will further increase the adoption of this life failure patients with left ventricular assist devices for
saving therapy. destination therapy. Circulation: Heart Failure. 2012;
5: 241–248.
Patlolla B, Beygui R, Haddad F. Right-ventricular failure
Further Reading following left ventricle assist device implantation.
Cheng JM, Den Uil CA, Hoeks SE, et al. Percutaneous left Current Opinion in Cardiology. 2013; 28: 223–233.
ventricular assist devices vs intra-aortic balloon pump Rose EA, Gelijns AC, Moskowitz AJ, et al. Randomized
counterpulsation for treatment of cardiogenic shock: a Evaluation of Mechanical Assistance for the Treatment
meta analysis of controlled trials. European Heart of Congestive Heart Failure (REMATCH) Study
Journal. 2009; 30: 2102–2108. Group. Long-term mechanical left ventricular
Gilotra NA, Stevens GR. Temporary mechanical circulatory assistance for end-stage heart failure. New England
support: a review of the options, indications, and Journal of Medicine. 2001; 345: 1435–1443.
outcomes. Clinical Medical Insights: Cardiology. 2014; Slaughter MS, Pagani, FD, McGee EC, et al.
8(Suppl 1): 75–85. HeartWare ventricular assist system for bridge to
Kirklin JK, Naftel DC, Kormos RL, et al. Fifth transplant: combined results of the bridge to transplant
INTERMACS annual report: risk factor analysis from and continued access protocol trial. Journal of Heart
more than 6,000 mechanical circulatory support and Lung Transplantation. 2013; 32: 675–683.
patients. Journal of Heart and Lung Transplantation. Stevenson LW, Pagani FD, Young JB, et al. INTERMACS
2013; 32: 141–156. profiles of advanced heart failure: the current picture.
Mancini D, Colombo PC. Left ventricular assist devices. Journal of Heart and Lung Transplantation. 2009;
a rapidly evolving alternative to transplant. Journal 28: 535–540.
of the American College of Cardiology. 2015; Uriel N, Han J, Morrison KA, et al. Device thrombosis in
65: 2542–2555. HeartMate II continuous-flow left ventricular assist
Park SJ, Milano CA, Tatooles AJ, et al. HeartMate II devices: a multifactorial phenomenon. Journal of Heart
Clinical Investigators. Outcomes in advanced heart and Lung Transplantation. 2014; 33: 51.
MCQs
1. A 55 year old man with dilated cardiomyopathy pre- 2. A 48 year old man presents with recent onset short-
sents with signs of advanced heart failure and severe ness of breath at rest and paroxysmal nocturnal dysp-
left ventricular dysfunction. He is blood group O and noea. His blood group is A. His echocardiogram
has a body mass index of 26. His right heart catheter shows severe left ventricular systolic dysfunction
measured a transpulmonary gradient of 8 mmHg, with an ejection fraction of 16%, probably second-
pulmonary vascular resistance of 3 Wood units and ary to dilated cardiomyopathy. Pulmonary function
cardiac index of 1.6 l m−2. He has remained inotrope tests and coronary angiogram were satisfactory. Right
dependent despite several attempts at weaning and heart catheter showed normal pulmonary artery pres-
his renal function is normal. He does not have signs sure and a transpulmonary gradient of 6 mmHg. His
of sepsis. He has been on the urgent heart transplant cardiopulmonary exercise test showed peak oxygen
waiting list for 10 weeks with no suitable offers. His uptake (VO2 max) of 12 ml kg−1 min−1 and his brain
best therapeutic option is: natriuretic peptide (BNP) is 4500 pg ml−1. He has
(a) Continue on inotropic support indefinitely until a peripheral oedema and is on maximum diuretic ther-
donor heart becomes available apy. His therapeutic best option is:
(b) Insert intra-aortic balloon pump and wait (a) Continue medical management and listing for
indefinitely until a donor heart becomes heart transplantation
available
(b) Consider intravenous inotropic therapy
(c) Consider implantation of long term LVAD, dis-
charge him into the community and have an active (c) Consider putting him on ECMO support
life until a donor heart becomes available (d) Consider putting him on short term Bi-VAD
(d) Refer him to palliative care support
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3. A 44 year old male with a 2 week history of angina was are deranged with elevated prothrombin time and
admitted with an anterior ST elevation myocardial elevated serum creatinine. He is inotrope dependent
infarction (STEMI). He was taken to the cathlab for a and no further improvement is evident despite IABP
percutaneous intervention to a lesion in his left main insertion. The best therapeutic option is:
stem coronary artery. During this procedure, he devel-
(a) Continue to optimise medical therapy and wait for
oped severe hypotension and circulatory collapse,
him to improve
which was unresponsive to boluses of epinephrine
or insertion of an intra-aortic balloon pump (IABP). (b) Insert long term LVAD
He went on to have a cardiac arrest in the cathlab and (c) Urgently list for heart transplant
external cardiac compressions were commenced to
maintain circulation. His best therapeutic option is: (d) Insert Bi-VAD (LVAD and RVAD) as a bridge to
candidacy and once his end organ function recov-
(a) Continue external cardiac massage to maintain ers, list him for urgent heart transplant
circulation
5. A 68 year old female with type II diabetes presents
(b) No therapeutic options are available in such
with a history of angina, triple vessel coronary artery
extreme situations
disease and severe left ventricular dysfunction. She
(c) Emergency sternotomy and internal cardiac underwent elective coronary artery bypass grafting
massage using the left internal mammary artery and two long
(d) Institution of extracorporeal life support (ECLS) as saphenous vein grafts on cardiopulmonary bypass.
bridge to decision On coming off bypass, she became hypotensive and
a transoesophageal echocardiogram demonstrated
4. A 51 year old male, blood group O, previously fit global left ventricular hypokinaesia. The bypass
and well, presents with a short history of breathless- grafts are patent and she was started on inotropes
ness, right upper quadrant abdominal pain and gross with little effect. What should be the next line of
peripheral oedema. On examination, he was clinically action?
jaundiced. His echocardiogram shows severe biven-
tricular dysfunction. His angiogram shows normal (a) Insertion of intra-aortic balloon pump
coronaries. A right heart catheter shows right atrial (b) Short term LVAD
pressure of 18 mmHg, mean pulmonary artery pres-
(c) Long term LVAD
sure of 28 mmHg, a wedge pressure of 18 mmHg and
PVR of 4.5 Wood units. Liver and renal functions (d) Institution of ECMO
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Cardiac Extracorporeal Membrane

Chapter
23 Oxygenation
Jason M Ali and David P Jenkins
Extracorporeal membrane oxygenation (ECMO) is Table 23.1 Indications for cardiac ECMO

an advanced form of temporary life support to aid Acute myocardial infarction
respiratory and/or cardiac function that has been in Dilated cardiomyopathy
existence since the 1970s. ECMO evolved from car- Fulminant myocarditis
diopulmonary bypass (CPB) technology and similarly
Cardiac failure due to intractable arrhythmias
involves diverting venous blood through an extracor-
Postcardiotomy cardiac failure
poreal circuit, in which gaseous exchange occurs, and
returning it to the body. Early experience with ECMO Primary graft failure following cardiac transplantation
was plagued by high complication rates and an ina- Acute heart failure secondary to drug toxicity
bility to demonstrate a survival benefit over conven-
tional management, leading to it being reserved as a balloon counterpulsation. Common causes of such
last-resort treatment, initiated when death was a near cardiogenic shock are included in Table 23.1.
certainty. Significant advances in ECMO technology Concomitant respiratory failure is not an abso-
and experience have resulted in the technique becom- lute requirement for considering cardiac ECMO over
ing safer and therefore part of the advanced manage- alternative mechanical circulatory support devices.
ment of severe cardiopulmonary disease. There have been no randomised controlled trials in
This chapter focuses on the use of ECMO in the adults that have compared VA ECMO against iso-
management of severe cardiac or cardiorespiratory lated ventricular support with a temporary ventricu-
failure. This is distinguished from ECMO used in lar assist device (VAD). However, the coexistence
respiratory failure by the site that oxygenated blood of respiratory indications such as severe refractory
is reinfused (which will be discussed in Chapter 24). hypoxia, hypercapnic respiratory failure or sympto-
When being used for the management of cardiac fail- matic pulmonary hypertension is certainly persuasive
ure, oxygenated blood is reinfused into the systemic in deciding to pursue cardiac ECMO instead of other
arterial circulation (venoarterial (VA) ECMO). In this circulatory support techniques. The advantages of
situation, both the heart and lungs are bypassed by the ECMO over alternative mechanical circulatory sup-
ECMO circuit. In contrast, when managing respira- port devices such as ventricular assist devices (VAD)
tory failure alone, oxygenated blood is reinfused into include the rapidity of insertion, the ability to support
a central vein (venovenous (VV) ECMO), bypassing biventricular failure at high flow rates and the poten-
only the function of the lungs, and the patient is still tial to support patients with concomitant lung injury
dependent on intrinsic cardiac function for develop- when required.
ing cardiac output. More recently, cardiac ECMO has also been used
to restore circulation during cardiac arrest refractory
Indication for Cardiac ECMO to standard resuscitative management (termed ‘extra-
Cardiac (VA) ECMO may be indicated in patients with corporeal cardiopulmonary resuscitation’ (eCPR)).
cardiogenic shock (impaired cardiac output resulting This may be beneficial when a witnessed arrest occurs
in end-organ dysfunction) that is refractory to maxi- in hospital, especially if the patient is in an intensive
mal conventional therapy with inotropic drugs and less care or cardiac catheter laboratory setting and ECMO
invasive mechanical support, for example intra-aortic can be instituted rapidly. Evidence suggests that
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outcome is best with resuscitation periods of less than Most commonly anticoagulation is with unfractionated
30 minutes although there are case reports of survival heparin, although there are reports of utilising newer
with far longer arrests. agents such as bivilirudin and argatroban in the con-
text of antithrombin III deficiency and heparin induced
Contraindications for Cardiac ECMO thrombocytopenia. Efforts are focused on developing a
truly biocompatible plastic, which will obviate the need
Deciding to commence ECMO is a major decision and
for anticoagulation which is responsible for a signifi-
ideally it should be multidisciplinary with involve-
cant proportion of ECMO complications.
ment of cardiology (and respiratory) physicians,
Blood flow through the circuit is driven by an
cardiothoracic surgeons and specialist intensivists.
external pump. Two types exist: simple roller-pumps
The difficulty is that the patient is often deteriorating
and constrained vortex centrifugal pumps.
rapidly in cardiogenic shock with an uncertain diag-
ECMO oxygenators are usually polymethylpen-
nosis and prognosis at the time the decision needs to
tene hollow-fibre devices, and modern devices have
be made. A delay in restoring blood pressure and flow
low resistance. Carbon dioxide is readily extracted via
can result in irrecoverable multiorgan failure despite
gradient-mediated mechanisms whilst the addition of
adequate ECMO flow. In many cases in critically ill
oxygen is slower due to its reduced solubility and dif-
patients, at the time of cannulation it is uncertain
fusion characteristics. An air/oxygen blender is used
whether organ function is recoverable and support is
to achieve the desired FiO2 and titrated based on arte-
expectant. Cardiac ECMO is not a long-term therapy
rial blood gases.
and should only be considered in patients with antici-
pated early recovery, or as a bridge to heart transplan-
tation or implantation of a long-term VAD. Cardiac Cannulation Strategies
ECMO is therefore contraindicated in patients with
irrecoverable cardiac failure who will not be candi- Peripheral Cannulation
dates for transplantation or VAD implantation and in Vascular access cannulae can be placed centrally,
patients with established multiorgan failure. as for CPB, or peripherally to establish VA ECMO
The following are considered relative contraindi- (Figure 23.1). They can be inserted by surgical cut-
cations to cardiac ECMO: the presence of severe aor- down under direct vision or percutaneously using the
tic regurgitation, aortic dissection, contraindications Seldinger technique under ultrasound guidance. The
to therapeutic anticoagulation (such as active bleed- most common configuration in adults is placement of
ing, a haemorrhagic intracranial event), pre-existent the venous drainage cannula in the femoral vein and
multiorgan failure and patients who have already been reperfusion cannula into the femoral artery. The axil-
mechanically ventilated for >10–14 days. lary/subclavian artery can also be utilised as an alterna-
Although there are no absolute guidelines on the tive arterial return vessel. Another strategy, commonly
indications and contraindications for cardiac ECMO, used in paediatric and neonatal ECMO, is the internal
the Extracorporeal Life Support Organisation (ELSO) jugular vein–common carotid artery cannulation.
and the European Extracorporeal Life Support (ECLS) Each strategy has important considerations.
Working Group have published recommendations for
the use of ECMO in critically ill patients. Femoral Artery Cannulation
This is associated with two main complications:
Circuit Design and Considerations 1. With this strategy, oxygenated blood is pumped
The ECMO circuit is similar for VV and VA use and in a retrograde direction up the descending
consists of vascular access cannulae, a pump, an oxy- aorta and into the ascending aorta to perfuse
genator, a temperature control system, monitors and the coronary arteries and cerebral vessels.
access points. However, this assumes that there is no residual
The vascular access cannulae and circuit tubing are left ventricular cardiac output. If there is native
made of a plastic, which therefore necessitates thera- cardiac output with the aortic valve opening,
peutic anticoagulation to prevent activation of the clot- there will be a ‘mixing zone’ where ejected native
ting cascade and thrombosis of the circuit. Heparin anterograde and reinfused retrograde blood meet
bonding of the material aims to reduce this activation. (Figure 23.2). This can cause a problem if, in the
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Chapter 23: Cardiac Extracorporeal Membrane Oxygenation
Ascending aorta
Left atrium
Pump
Right atrium
Right ventricle
Left ventricle
Oxygenator
Descending aorta
Inferior vena cava
Femoral artery
Femoral vein
Drainage cannula
Reperfusion line
Return cannula
Figure 23.1 Peripheral ECMO. The blood is drained from a large vein, typically IVC, using femoral access. It is then pumped through an
oxygenator and returned to the patient into the femoral artery in a retrograde fashion. A reperfusion line from the inflow cannula is inserted
into the distal femoral artery to provide distal limb perfusion. Diagram drawn by Anna Valchanova. (A black and white version of this figure
will appear in some formats. For the colour version, please refer to the plate section.)
context of respiratory failure, the blood exiting of an additional reinfusion catheter into the
the left ventricle is deoxygenated. This situation internal jugular vein such that a proportion
is not infrequent when left ventricular failure is of the oxygenated blood is reinfused into the
complicated by pulmonary oedema. As native pulmonary circulation (increasing the saturation
cardiac function recovers and left ventricular of antegrade ejected blood from the left ventricle).
ejection increases, if the mixing zone is within Alternatively, the femoral reinfusion cannula
the descending aorta, the coronary and cerebral could be resited proximally to the subclavian,
circulations may be exposed to deoxygenated common carotid or ascending aorta.
blood. Monitoring of cerebral saturations and 2. The second complication of femoral arterial
right radial artery blood gases can be indicative of cannulation is ipsilateral ischaemic limb injury
this ‘differential cyanosis’ or Harlequin syndrome. due to obstruction of distal femoral arterial blood
Strategies to manage this complication include flow that can lead to critical limb ischaemia
increasing ventilatory support in an attempt to necessitating fasciotomies or even amputation if
improve oxygenation of the pulmonary venous not recognised. This can be avoided by placement
blood, increasing the flow through the femoral of a small antegrade perfusion catheter into the
arterial catheter with the aim of transferring the superficial femoral artery distal to the ECMO
mixing zone to the ascending aorta, or placement cannula, to perfuse the leg.
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graft onto the artery that is then cannulated. The lat-

ter allows flow to continue distally to perfuse the arm.
Bleeding complications are relatively common from
the suture lines and occasionally the arm can become
hyperperfused with resulting severe swelling and
damage if venous return is compromised.
Carotid Artery Cannulation

With ligation of the carotid artery, there is an
increased risk of neurological injury, with dependence
on a complete circle of Willis for collateral circulation
to the brain.
Central Cannulation
Cardiac ECMO can also be instituted with central can-
nulation as for CPB (Figure 23.3). Central cannulation
is performed by cardiothoracic surgeons via a median
sternotomy. Larger catheters can be used which per-
mit increased flow rates and maximal haemodynamic
support with more certainty of the ECMO circuit tak-
ing over the whole of the patient’s circulation. This
approach is most commonly used if a sternotomy
has already been made, for example in patients with
postcardiotomy cardiac failure following cardiac sur-
gery or primary graft failure at transplantation. It is
occasionally necessary in patients where peripheral
access is not possible. There are also reports of this
strategy being used in cases of severe sepsis, taking
advantage of the greater haemodynamic support pos-
sible; however the requirement for sternotomy adds
to the potential complications and morbidity in these
Figure 23.2 Watershed phenomenon during venoarterial ECMO
visualised by computed tomography. Antegrade blood flow (low
patients. This approach necessarily involves a major
contrast) from the heart competes with retrograde blood flow surgical incision and therefore bleeding is the most
(high contrast) from the ECMO in the aorta, resulting in a watershed frequent problem. Usually institution of anticoagula-
phenomenon (arrowhead). Here computed tomography of a
patient with pulmonary embolism and reduced cardiac output
tion is delayed 6–12 hours until bleeding is controlled.
demonstrates a rather proximal watershed, leading to perfusion of
the right carotid artery with ‘heart blood’ (dark) and the left carotid
artery with ‘ECMO blood’ (bright, arrows). Upper panel, sagittal
General Management of Patients on
oblique maximum intensity projection (MIP); middle panel, coronal
oblique MIP; lower panel, transverse plane. From Napp et al. (2016).
Cardiac ECMO
Patients supported by cardiac ECMO should be man-
aged in an intensive care unit by multidisciplinary
Axillary/Subclavian Cannulation specialists. There are several important considerations
The main advantage of this strategy for arterial return that should be made when managing these patients,
is that the entry site for returned oxygenated blood is many of which are similar to patients supported by
more central in the aorta, so that more of the flow is ‘respiratory’ (VV) ECMO.
in the physiological antegrade direction, avoiding the The circulatory haemodynamics of patients must
potential for the first complication above. However, be closely monitored. ECMO support should be
there are also disadvantages. A surgical cut-down is titrated to clinical targets, which may include:
always needed, and it is usually necessary to sew a side • Arterial oxygen saturations >90%
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(a)
Ascending aorta
Drainage cannula
Left atrium
Return cannula
Pump
Right atrium
Right ventricle
Left ventricle
Oxygenator
Descending aorta
Inferior vena cava
(b)
Figure 23.3 (a) Central ECMO diagram: using open chest, the blood is drained via a cannula from a central vein (IVC or SVC) or right atrium.
It is pumped through an oxygenator and returned through an arterial cannula into the ascending aorta. The chest can be left open for a
short while, or the cannulae can be tunnelled under the skin and chest closed. Diagram drawn by Anna Valchanova. (b) A photograph of
the outflow and inflow cannulae secured with spigots. (A black and white version of this figure will appear in some formats. For the colour
version, please refer to the plate section.)
• Venous oxygen saturations >70% In most cases there is some residual ventricular func-
• Adequate tissue perfusion, as judged by tion, and it is beneficial for some pulsatility to con-
end-organ function and lactate levels. tinue. This allows emptying of the ventricles and less
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chance of distension and stasis. Low dose inotropic

support is sometimes required to achieve ventricular
Weaning Cardiac ECMO
It is important to develop an individual strategy for
ejection and aortic valve opening; the latter can be
all patients supported on VA ECMO. It will often be
confirmed by echocardiography. In cases of severe left
instituted as an emergency when the aetiology of cir-
ventricular dysfunction with no effective contraction,
culatory collapse and diagnosis may be unclear at the
peripheral cardiac ECMO can lead to overdistension
time. Cardiac ECMO support will only be possible
of the left ventricle and left atrium, worsening pulmo-
for 1–2 weeks and therefore ECMO in this situation
nary oedema. This can also lead to further myocardial
is a temporary support to recovery of heart function
injury. Serial echocardiography should be performed
or a bridge to another treatment. In some patients,
to monitor for this complication. If identified, several
weaning of support will not be possible, and after
strategies have been described to facilitate decom-
careful evaluation they may be candidates for urgent
pression, including addition of a vent cannula via the
cardiac transplantation or if donors are not available
left ventricular apex, or transseptal via the atrium,
a planned transfer to temporary or implantable ven-
increasing inotropic support, further mechanical sup-
tricular assist.
port such as Impella I or IABP, conversion to central
Patients are monitored for recovery of intrinsic
ECMO or alternative support modalities such as a
cardiac and respiratory function. Evidence of recov-
percutaneous VAD.
ery of left ventricular function can be assessed by
Anticoagulation must be monitored to prevent cir-
examining for pulsatility in the arterial line waveform
cuit thrombosis and embolism, which could be fatal.
and by echocardiography. In conjunction, for patients
For patients receiving unfractionated heparin, an
with concomitant respiratory failure, improvements
activated clotting time (ACT) of 180–210 seconds is
in arterial oxygen saturation, pulmonary compliance
recommended, which is lower than the >400 seconds
and chest radiography can suggest recovery of res-
recommended for CPB.
piratory function. Weaning of cardiac ECMO is more
Lung protective ventilation is usually adopted
complicated than in the case of VV ECMO, where
to minimise barotrauma and volutrauma. Positive
titration is against gas exchange alone, as in most cases
end expiratory pressure is applied to the lungs to
both the heart and lungs have been supported and it is
maintain alveolar recruitment, but the ventilator is
not safe to have a prolonged trial off support prior to
usually set to low tidal volumes, low inspiratory pres-
decannulation.
sures and a low inspired oxygen fraction. Reduction
Once adequate recovery is thought to have
in the ventilator support is often accompanied by
occurred, an attempt to wean off ECMO can be made.
increased venous return and cardiac output. This
This is usually accomplished by successive reduction
strategy is found to help prevent ventilator induced
in flow of approximately 0.5 l on a daily basis, until
lung injury, oxygen toxicity and ventilator associ-
the ECMO support is only 1.5–2.0 l/min. During this
ated haemodynamic compromise. Indeed, preven-
time, careful assessment of end- organ function is
tion of further lung injury in these patients is one
vital. Most patients will also require additional ino-
of the major advantages of cardiac ECMO. However,
tropic support. Final decannulation usually occurs in
it is important to remember that in patients with
the operating room as formal vessel repair for periph-
improving ventricular function, more blood will be
eral cannulation, and chest closure for central cannu-
ejected from the right ventricle into the pulmonary
lation is required. For circuits with a bridge between
circulation and increased ventilation will be neces-
the inflow and outflow limbs, the arterial and venous
sary to prevent deoxygenated blood reaching the left
catheters can be clamped, leaving blood circulating
atrium.
through the external circuit through the bridge. If
The most comprehensive guidelines on the man-
a bridge is not present, flow through the circuit can
agement of patients on ECMO are published by ELSO.
be reduced to a minimal setting to prevent stasis. In
These provide guidance on the use of ECMO includ-
both cases it is essential to ensure therapeutic anti-
ing training, resources and quality assurance. They are
coagulation due to the increased risk of thrombosis
not intended to represent a standard of care, however,
with reduced flow. During the final trial off ECMO
and practice described in the literature often differs in
completely, the patient is monitored for adequate
parts from this guidance.
cardiorespiratory function.
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Should cardiac function begin to recover but Table 23.2 Complication rates of cardiac ECMO
respiratory failure persists, it is important to ensure
Complication Incidence (%)
adequate oxygenation of the coronary and cerebral
Acute kidney injury 55.6
circulation and such patients may need to be con-
verted to respiratory ECMO. Renal replacement therapy 46.0
Rethoracotomy for bleeding or 41.9
Complications tamponade in postcardiotomy patients

Major or significant bleeding 40.8
Although cardiac ECMO can improve the survival of
Significant infection 30.4
patients with advanced heart disease, these benefits
must be weighed against the significant associated Lower extremity ischaemia 16.9
morbidity. The major complications are haemorrhagic Neurological complications 13.9
or thrombotic, emphasising the importance of closely Fasciotomy or compartment syndrome 10.3
monitoring the level of anticoagulation –although Stroke 5.9
there is no universally accepted anticoagulation pro- Lower extremity amputation 4.7
tocol. Cardiac or major vascular perforation is a rare
but potentially lethal complication of cannulation, and
despite advances in equipment and technique, distal designing randomised controlled trials of life support
malperfusion remains a problem with peripheral can- that are ethically acceptable. As such, evidence is pri-
nulation. Mechanical equipment failure is now very marily from case series, cohort studies and registry data.
uncommon with modern ECMO circuits.
Acute kidney injury (AKI) occurs in around half Extracorporeal Life Support Organisation
of patients supported by ECMO. This is important
since AKI on ECMO is a marker of disease severity
Registry
and is associated with increased mortality. As such, The Extracorporeal Life Support Organisation (ELSO)
continuous renal replacement therapy has evolved was founded in 1989. This organisation maintains
into an adjunct support in patients on ECMO, with an international registry of patients who have been
the advantage of permitting correction of metabolic treated with all types of extracorporeal life support.
and fluid disturbances, and it may also suppress The results of the registry are published biannually
inflammation by counteracting the systemic inflam- and distributed to members. As of July 2015 a total
matory response. of 69,114 patients (including neonatal, paediatric
A recent meta-analysis summarised complications and adult) are included in the registry, with a total of
of cardiac ECMO from 20 studies reporting on out- 20,236 patients having been on cardiac ECMO and a
comes in 1866 patients. The complication rates they further 5756 patients having eCPR. The registry data
reported are summarised in Table 23.2. report that for cardiac ECMO, 62% of patients sur-
For survivors of ECMO, there has been the sug- vived extracorporeal life support and 45% survived to
gestion that there is an increase in neurological defi- discharge or transfer.
cits and respiratory morbidities, and for the neonatal/ In general, the survival for cardiac ECMO in
paediatric population neurodevelopmental deficits adults is inferior to the survival for respiratory
and behavioural problems. However, more recent ECMO. Patients supported postcardiotomy or as part
data comparing non- ECMO arms of randomised of extended CPR have the worst survival. The chance
controlled trials have observed no between- group of overall survival is determined by the diagnosis,
differences for these outcomes. Patients who survive state of end-organ damage at the time of initiation of
ECMO require prolonged rehabilitation and multidis- support, and in the case of non-recovery the potential
ciplinary follow-up after discharge from hospital. for cardiac transplantation or more permanent ven-
tricular support.
Outcomes and Evidence
There is a paucity of evidence demonstrating the abso- Future Direction
lute benefit of cardiac ECMO in improving survival or The improvement in ECMO technology over the
quality of life. This is partially due to the difficulty of last 10 years has allowed greater adoption of cardiac
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ECMO and use in expanding areas including acci- in patients who have recoverable cardiac disease
dent and emergency, cardiac surgery, and PCI cath- or who are candidates for transplantation or
eter labs. There has also been a steady increase in the implantation of a ventricular assist device.
use of ECMO during cardiopulmonary resuscitation • In adults, most commonly, venous blood is
(eCPR). drained via a catheter in the femoral vein and
Although there are no randomised controlled tri- reinfused oxygenated via a catheter in the femoral
als, there is increasing evidence of efficacy. A pro- artery, therefore bypassing both cardiac and
spective observational study of witnessed in-hospital respiratory function. Post cardiotomy, central
cardiac arrest, with propensity matched controls, dem- cannulation is often utilised.
onstrated significantly higher survival to discharge and • Cannulation of the femoral artery can be
at 1-year follow-up in the eCPR group. There is some complicated by ipsilateral ischaemic limb injury,
evidence that combining eCPR with primary percuta- and can also result in the phenomenon of
neous coronary intervention for acute coronary syn- ‘differential cyanosis’ with good oxygenation of
dromes improves likelihood of successful outcomes. the lower body, but with ejection of deoxygenated
Although data are supportive, overall survival is low blood to the upper body.
with only 30% of adults surviving to discharge in the • Complications of cardiac ECMO are
ELSO registry data. More research is required to define largely related to the need for therapeutic
the patient population that will derive the greatest anticoagulation, the major complications being
benefit from eCPR with an emphasis on survival with thrombotic or haemorrhagic. Almost half of the
minimal neurological impairment. patients on cardiac ECMO develop acute kidney
Developments in the technology continue to be injury, which is associated with a poorer outcome.
made with the goal of lowering complication rates, • Much of the evidence supporting the use of
allowing more patients to benefit. The goal of develop- cardiac ECMO is based on small observational
ing antithrombogenic materials requiring no antico- studies and the international registry held by
agulation will be a big advance in ECMO technology the Extracorporeal Life Support Organisation
that is likely to significantly reduce morbidity. (ELSO). Randomised controlled trials are
One challenge that remains with the management required to expand the evidence base for this
of patients on ECMO is discontinuation of support in therapy. Overall survival is poor and reflects the
patients with irreversible disease and no other option. severity of the disease state necessitating support.
As technology and experience increase, patients can be
managed on ECMO for longer and so futility becomes
more difficult to define. In order to facilitate use of
Further Reading
this technology in an appropriate and cost effective Abrams D, Combes A, Brodie D. What’s new in
manner, better predictors of outcome are necessary. extracorporeal membrane oxygenation for cardiac
failure and cardiac arrest in adults? Intensive Care
Despite the increasing use of ECMO for advanced
Medicine. 2014; 40: 609–612.
cardiopulmonary disease, many questions remain
unanswered and the benefit over conventional therapy Beckmann A, Benk C, Beyersdorf F, et al. Position article
for the use of extracorporeal life support in adult
has yet to be conclusively demonstrated. To date, the patients. European Journal of Cardio-Thoracic Surgery.
highest level of evidence for cardiac ECMO is limited 2011; 40: 676–680.
to cohort studies. In view of this paucity of data sup-
Bembea MM, Annich G, Rycus P, et al. Variability
porting the benefit of ECMO, there is a need for large in anticoagulation management of patients
randomised controlled trials to better define the use of on extracorporeal membrane oxygenation: an
this advanced life support. Such studies would ideally international survey. Pediatric Critical Care Medicine.
include cost-benefit analyses to better quantify the 2013; 14: e77–84.
economic impact of this resource intensive therapy. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary
resuscitation with assisted extracorporeal life-support
Learning Points versus conventional cardiopulmonary resuscitation in
adults with in-hospital cardiac arrest: an observational
• Cardiac ECMO is an advanced life support study and propensity analysis. Lancet. 2008;
technique used in refractory cardiogenic shock 372: 554–561.
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Cheng R, Hachamovitch R, Kittleson M, et al. oxygenation in adults with cardiogenic shock.

Complications of extracorporeal membrane Circulation. 2015; 131: 676–680.
oxygenation for treatment of cardiogenic shock Napp CL, Kühn C, Hoeper MM, Vogel-Claussen J,
and cardiac arrest: a meta-analysis of 1,866 Haverich A, Schäfer A, et al. Cannulation strategies for
adult patients. Annals of Thoracic Surgery. 2014; percutaneous extracorporeal membrane oxygenation
97: 610–616. in adults. Clinical Research in Cardiology. 2016;
Extracorporeal Life Support Organisation. General 105: 283–296.
Guidelines for all Extracorporeal Life Support, version Tramm R, Ilic D, Davies AR, Pellegrino VA, Romero L,
1.3. Ann Arbor MI, 2013. Hodgson C. Extracorporeal membrane oxygenation
Gaffney AM, Wildhirt SM, Griffin MJ, Annich GM, for critically ill adults. Cochrane Database of Systematic
Radomski MW. Extracorporeal life support. British Reviews. 2015; 1: CD010381.
Medical Journal. 2010; 341: c5317. Werdan K, Gielen S, Ebelt H, Hochman JS. Mechanical
Lawler PR, Silver DA, Scirica BM, Couper GS, Weinhouse circulatory support in cardiogenic shock. European
GL, Camp (Jr) PC. Extracorporeal membrane Heart Journal. 2014; 35: 156–167.
MCQs
1. When monitoring a patient supported on VA periph- (c) Possible malignancy
eral ECMO with cannulation of the femoral vessels, (d) Mechanical ventilation for 7 days
arterial blood gases should be taken from where to
best reflect patient oxygenation? (e) Recent cardiac surgery
(a) Contralateral femoral artery 4. Compared with peripheral VA ECMO, central cannu-
lation results in:
(b) Right radial artery
(a) Less drainage and emptying of the heart
(c) Left radial artery
(b) Lower chance of left ventricular recovery
(d) ECMO circuit post oxygenator
(c) A lower risk of bleeding
(e) ECMO circuit pre oxygenator
(d) More native flow in the pulmonary arteries
2. Which of the following is not a strategy that can be
used to manage ‘differential cyanosis’ due to return of (e) A more proximal mixing zone in the aorta
native cardiac function? 5. According to the Extracorporeal Life Support
(a) Increase ventilator support Organisation (ELSO) registry, what percentage of
patients receiving ECMO as part of cardiopulmonary
(b) Decrease the flow through the arterial reinfusion resuscitation (eCPR) survive to discharge?
catheter
(a) 10%
(c) Insertion of an additional internal jugular venous
reinfusion cannula (b) 20%
(d) Re-site the reinfusion catheter into a more (c) 30%
proximal artery (d) 40%
(e) Vent the left heart to improve drainage (e) 50%
3. Which of the following is considered a relative con-
traindication to commencement of cardiac ECMO?
(a) Aortic stenosis
(b) Aortic dissection
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Respiratory Extracorporeal Membrane

Chapter
24 Oxygenation in the Cardiothoracic

Intensive Care Unit
Darryl Abrams and Daniel Brodie
Introduction When blood is drained from a vein and returned

to an artery, it is referred to as venoarterial ECMO,
Although extracorporeal membrane oxygenation
and the circuit is able to provide both respiratory
(ECMO) was first introduced in the 1970s as a means
and circulatory support. The amount of blood flow
of supporting severe impairments in gas exchange,
through the circuit (including the fraction of ECMO
original versions of the technology were associated
blood flow relative to the amount of native cardiac
with high device related and patient related compli-
output), the fraction of oxygen delivered through
cation rates, particularly thrombosis and haemor-
the gas compartment of the oxygenator (referred to
rhage, with no evidence of benefit over conventional
as the FDO2), and native lung function are the main
management strategies at the time. Recent advances
determinants of systemic oxygenation for patients
in ECMO technology have improved its risk-benefit
supported with ECMO. The rate of gas flow through
profile, and a growing body of literature in the con-
the oxygenator, known as the sweep gas flow rate,
text of greater experience with its use has sparked a
and, to a lesser degree, the blood flow rate are the
renewed interest in the use of ECMO for respiratory
major determinants of carbon dioxide removal.
failure. This chapter will review the basic principles
Extracorporeal circuits are more efficient at carbon
underlying the use of ECMO, cannulation strategies,
dioxide removal than oxygenation, owing to the dif-
indications and evidence for ECMO in the setting of
fusion properties of the membrane and the manner
respiratory failure, as it pertains to the cardiothoracic
in which oxygen and carbon dioxide are transported
intensive care unit. Beyond the current considerations
within the blood. Because carbon dioxide can be
for ECMO, we will explore emerging indications that
effectively removed at lower blood flow rates than
could change the approach to the management of res-
those typically required for oxygenation, it may be
piratory failure in the intensive care unit in the future.
possible to use smaller cannulae, which in turn may
be easier and safer to insert. The technique of extra-
Basic Principles corporeal support for carbon dioxide removal at low
ECMO refers to an extracorporeal circuit that directly blood flow rates is referred to as extracorporeal car-
oxygenates and removes carbon dioxide from the bon dioxide removal (ECCO2R). This approach has
blood via an oxygenator, a device that consists of a the potential to support patients with acute hyper-
semipermeable membrane that selectively permits capnic respiratory failure and to facilitate reductions
oxygen and carbon dioxide to diffuse between blood in tidal volumes and airway pressures in the acute
and gas compartments. Deoxygenated blood is with- respiratory distress syndrome that would otherwise
drawn through a drainage cannula via an external be limited by unacceptable levels of respiratory aci-
pump, typically a centrifugal pump, which creates dosis. An alternative, pumpless configuration that is
negative pressure within the drainage cannula and less frequently employed is arteriovenous ECCO2R
tubing. The blood passes through the oxygenator, (blood drained from a femoral artery and returned to
where gas exchange occurs, and is returned to the the contralateral femoral vein), in which the patient’s
patient through a reinfusion cannula under posi- native cardiac output generates blood flow through
tive pressure. When blood is both drained from and an oxygenator. Because extracorporeal blood flow
returned to a vein, it is referred to as venovenous tends to be lower, this approach is usually limited to
ECMO and provides only gas exchange support. the modulation of carbon dioxide.
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Chapter 24: Respiratory Extracorporeal Membrane Oxygenation
Cannulation Configurations Indications and Evidence

Traditionally, venovenous ECMO is implemented
by cannulation of a femoral vein for drainage and Severe Acute Respiratory Distress Syndrome
an internal jugular vein for reinfusion (Figure 24.1). The acute respiratory distress syndrome (ARDS)
This configuration may result in directing reinfused remains among the most common indications for
oxygenated blood toward the port of the drainage ECMO for respiratory failure worldwide, although
cannula. The phenomenon of drawing reinfused, oxy- evidence supporting its use remains limited. Positive
genated blood back into the circuit without passing pressure ventilation, although often necessary for more
through the systemic circulation is known as recircu- severe forms of ARDS, is known to exacerbate lung
lation, which may negatively impact the effect of the injury, and a ventilation strategy that targets low tidal
ECMO circuit on systemic oxygenation. The develop- volumes and airway pressures has been established as
ment of the bicaval dual lumen cannula (Figure 24.2) one of the few interventions that improves outcomes
has enabled the implementation of venovenous in ARDS, along with prone ventilation. The poten-
ECMO through a single vein, with the advantages – tial role for ECMO in ARDS is two-fold. In patients
when positioned properly –of less recirculation and with respiratory failure so severe that the ventilator
avoidance of femoral cannulation. In order to opti- is insufficient to support gas exchange (or can do so
mise blood flow and recirculation, cannulation typi- only at the expense of unacceptably high airway pres-
cally requires imaging guidance to ensure that the tip sures), ECMO may serve as salvage therapy to manage
of the cannula is properly positioned in the inferior refractory hypoxaemia or hypercapnia. Alternatively,
vena cava and that the reinfusion jet is directed toward in patients whose respiratory system compliance is so
the tricuspid valve. The choice of cannula size is based severely reduced that standard-of-care low tidal vol-
on the physiological needs and size of the patient, and ume ventilation cannot be achieved due to unaccep-
consideration should also be made for any history of table levels of respiratory acidosis, ECMO (or more
chronic indwelling central venous catheters that may specifically ECCO2R) can facilitate reductions in tidal
have led to stenosis within the venous system. volumes by correcting the associated hypercapnia.
Figure 24.1 Peripheral VV ECMO

using two cannulae. Blood is
drained from the IVC using femoral
Return cannula approach. It is then pumped through
an oxygenator and returned into
the SVC through internal jugular
approach. Diagram drawn by Anna
Valchanova. (A black and white
version of this figure will appear in
some formats. For the colour version,
Oxygenator please refer to the plate section.)
SVC
IVC
Pump
Drainage cannula
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Drainage cannula
Return cannula
Inlet for SVC blood

(to circulate)
Pump
Outlet into right

atrium (from circuit)
Inlet for IVC blood

(to circulate)
Oxygenator
Descending aorta
Inferior vena cava
Figure 24.2 V VECMO using bicaval dual lumen cannula. Blood is drained from the IVC and SVC. It is pumped through an oxygenator and
returned into the right atrium using the second lumen of the same cannula. Diagram drawn by Anna Valchanova. (A black and white version
of this figure will appear in some formats. For the colour version, please refer to the plate section.)
As previously stated, the evidence support- ECMO, only 76% ultimately received ECMO, mak-
ing ECMO for ARDS has significant limitations. ing it difficult to quantify the effect of ECMO itself on
Prospective randomised controlled trials in the era outcomes. One reasonable conclusion to draw from
of early device technology failed to show a benefit this study is that referral to an ECMO-capable centre
to ECMO in severe ARDS, with high mortality rates may improve outcomes when compared with usual
in both arms. In the first randomised trial with rela- care in that setting. Non-randomised observational
tively modern ECMO technology for ARDS, entitled studies have shown conflicting results of the impact
Conventional Ventilation or ECMO for Severe Adult of ECMO on survival in severe ARDS, with a large
Respiratory Failure (CESAR), 180 subjects with amount of data derived from the influenza A (H1N1)
severe, potentially reversible respiratory failure were epidemic. Propensity analysis of patients in the UK
randomised to conventional mechanical ventilation matched on their likelihood of receiving ECMO for
or referral to a specialised centre for consideration severe ARDS due to influenza suggested a mortality
of ECMO. Subjects referred for consideration of benefit from ECMO (24% versus 47%, relative risk
ECMO, compared to those receiving conventional 0.51; 95% CI 0.31–0.84, p = 0.008). These findings
management, had a significantly lower rate of death contrast with other matched propensity analyses
or severe disability at 6 months (37% versus 53%, RR from a separate but similar French cohort, highlight-
0.69, p = 0.03). These findings must be interpreted ing the limitations of non-randomised retrospec-
with caution given limitations in study design. tive studies. To help address the role and impact of
Because it was designed as a pragmatic study, lung- ECMO on patients with severe ARDS, the ECMO to
protective ventilation was recommended but not Rescue Lung Injury in Severe ARDS (EOLIA) trial
mandated for the conventional arm, and only 70% of is being conducted; patients who remain in severe,
those subjects received such a strategy at any point in refractory ARDS despite optimal standard of care
the study. Among those referred for consideration of ARDS management (including low tidal volume
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ventilation, with the option for prone positioning, Analysis of the ARDS Network’s ARMA trial of con-
neuromuscular blockade and other rescue therapies) ventional (12 ml per kg and plateau airway pressure
are randomised to either ECMO or ongoing conven- <50 cmH2O) versus low tidal volume ventilation (6
tional support. ml per kg, plateau airway pressure <30 cmH2O) that
Several prognostic scores have been proposed in established the current standard of care for ventilation
order to identify patients most likely to benefit from strategies in ARDS suggests that subjects in the con-
ECMO in ARDS. The Predicting Death for Severe ventional group would have benefited from tidal vol-
ARDS on VV- ECMO (PRESERVE) score, which ume reduction regardless of plateau pressure quartile.
attempts to predict 6 month survival based on sev- A prospective cohort study has demonstrated an inde-
eral pre-ECMO measurements (age, body mass index, pendent linear relationship between lower tidal vol-
immunocompromised status, prone position, days of ume and decreased mortality that extends below 6 ml
mechanical ventilation, sepsis related organ failure per kg. Reductions in tidal volumes (from 6.3 ml per
assessment (SOFA), positive end- expiratory pres- kg to 4.2 ml per kg) and plateau airway pressures (from
sure (PEEP) and plateau pressure), was externally 29.1 to 25 cmH2O) with the assistance of ECCO2R to
validated in a cohort of venovenous ECMO patients, manage hypercapnia and acidaemia have been shown
with an AUC of 0.75 (95% CI 0.57 to 0.92; p = 0.01). to reduce inflammatory markers associated with lung
A more recent prediction model that utilised a com- injury in a single-centre cohort of patients with ARDS.
bination of pre-ECMO and ECMO day 1 data in a In a more recent clinical trial comparing ECCO2R
cohort of subjects receiving venovenous ECMO for assisted very low tidal volume ventilation (approxi-
severe ARDS demonstrated high discrimination with mately 3 ml per kg predicted body weight) to conven-
an area under curve of 0.79 (p = 0.03). With negative tional low tidal volume ventilation (approximately 6
and positive predictive values of 81% and 82%, this ml per kg) in patients with moderate to severe ARDS,
model performed better than several other proposed those with more severe hypoxaemia were found in post
scoring systems, including the PRESERVE score. hoc analysis to have a greater number of ventilator-free
Beyond short-term mortality prediction modelling, days when very low tidal volumes were used (40.9 ver-
little is known about the long-term functional, neuro- sus 28.2, p = 0.033). Two prospective randomised trials
cognitive and psychiatric outcomes of ARDS survivors comparing very lung protective ventilation to stand-
who received ECMO. Existing data suggest that such ard of care ventilation practices in less severe forms of
patients may have similar or potentially worse long-term ARDS or hypoxaemic respiratory failure are currently
neuropsychiatric sequelae compared with those who being designed and conducted, and may help to deter-
did not receive ECMO, though differences in severity of mine whether such a strategy translates into reductions
critical illness probably contribute to such findings. in lung injury and improvement in clinical outcomes.
Less Severe Forms of ARDS Acute Hypercapnic Respiratory Failure

Aside from its ability to support refractory hypoxae- Because of the relative ease with which ECCO2R can
mic or hypercapnic respiratory failure in severe ARDS, correct hypercapnia at lower blood flow rates than are
ECMO may have the benefit of reducing lung injury needed to provide oxygenation, there is great promise
even further than the current standard of care by facili- in using ECCO2R for the management of acute hyper-
tating the implementation of very low tidal volumes, capnic respiratory failure, potentially eliminating
airway pressures and respiratory rates through the the need for invasive mechanical ventilation in some
use of ECCO2R. This strategy, sometimes referred to patients. In COPD, the use of the ventilator is associ-
as ‘lung rest’, or ‘ultra-protective’ ventilation, is already ated with multiple complications, including dynamic
practised at many ECMO centres for patients with hyperinflation and elevations in intrinsic PEEP, venti-
severe ARDS, and additional research is being con- lator associated pneumonia, and impaired delivery of
ducted to systematically characterise current ventila- aerosolised medications, and failure of non-invasive
tion practices for these patients in order to help guide ventilation requiring invasive mechanical ventilation
optimal management strategies. Data demonstrating is associated with mortality as high as 30%. Several
the efficacy of such an approach, which may extend to case series and cohort studies have demonstrated
less severe forms of ARDS, are limited but promising. the feasibility of avoidance of or rapid weaning from
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invasive mechanical ventilation, with ECCO2R used of endotracheal extubation and early mobilisation
to manage gas exchange. In a matched cohort study may further improve outcomes and prevent loss of
of acute exacerbations of COPD comparing the com- transplant eligibility due to deconditioning. A major
bination of non- invasive ventilation plus ECCO2R limitation to the use of ECMO for end-stage respira-
to historical controls receiving non-invasive ventilatory failure remains the lack of a destination device
tion alone, the ECCO2R group had a significantly therapy. Patients with severe, irreversible respiratory
lower risk of intubation (HR 0.27; 95% CI, 0.07–0.98, failure, who are not lung transplant candidates, should
p = 0.047), though there was a high adverse event rate therefore not be offered ECMO.
related to ECCO2R. The rate of adverse events in this Primary graft dysfunction (PGD) is a form of acute
study may also have been related, in part, to the spe- lung injury that is the leading cause of early death after
cific device used. Additional benefits of ECCO2R over lung transplantation. Similar to its ability to support
mechanical ventilation may include increased suc- gas exchange in ARDS, ECMO may be used to man-
cess with early mobilisation. Although safety of early age PGD while underlying causes are treated and the
mobilisation during invasive mechanical ventilation allograft recovers. ECMO supported severe PGD may
has been well documented, it may have even greater have comparable survival to less severe PGD without
success with ECCO2R because of better control of ECMO support, particularly when instituted early,
dyspnoea with ECCO2R. Ultimately, more data are though long-term effects on allograft function have
needed to identify patients most likely to benefit from not been reported.
this overall approach, as well as the cost effectiveness
of such a strategy, before it should be implemented
outside the research setting. The benefit of ECCO2R Pulmonary Vascular Disease
in hypercapnic respiratory failure may extend beyond ECMO is an emerging management option in decom-
COPD, particularly for patients with refractory status pensated pulmonary hypertension with concomitant
asthmaticus, where the avoidance of positive pressure right ventricular failure. In patients with an iden-
ventilation is preferred. tifiable and reversible aetiology for decompensa-
tion, ECMO may offer an opportunity to correct gas
Lung Transplantation and Primary Graft exchange abnormalities and unload the right ventricle
while the underlying process is treated and directed
Dysfunction pulmonary hypertension therapies are initiated or
ECMO had long been considered a relative contrain- optimised. In patients with irreversible decompensa-
dication to lung transplantation because of poor tion who are transplant candidates, ECMO can serve
outcomes, especially when used as salvage therapy as a bridge to lung transplantation. The configuration
for patients failing invasive mechanical ventilation. typically used for decompensated pulmonary hyper-
However, in the era of improved technology and ear- tension is femoral venoarterial ECMO. A venoarte-
lier implementation, recent studies have reported rial approach decompresses the right ventricle and
improved post-transplant survival, particularly when results in reinfusion flow bypassing the pulmonary
performed at centres with more extensive experience. vasculature. Alternative configurations include: the
In a systematic review of 441 patients across 14 stud- use of a bicaval dual lumen cannula in patients with
ies supported with ECMO (the majority of whom pre-existing interatrial defects, where the reinfusion
were also receiving invasive mechanical ventilation) jet is directed across the defect, creating an oxygen-
while awaiting transplantation, mortality and 1-year ated right-to-left shunt; an upper body venoarterial
survival ranged from 10% to 50% and 50% to 90%, approach with the combination of internal jugular
respectively. The heterogeneity of patients and out- venous drainage and subclavian arterial reinfusion
comes suggests that patient selection and bridging via a graft, as discussed above; and pumpless arterio-
technique are probably important factors in opti- venous ECMO inserted between the main pulmonary
mising post-transplant survival. Given the potential artery and the left atrium, though this strategy typi-
for complications from invasive mechanical ventila- cally requires a sternotomy.
tion, a non-intubated ECMO strategy may be con- Acute massive pulmonary embolism may like-
sidered for select transplant candidates who would wise benefit from ECMO. Although there are no
otherwise be ventilator dependent. The combination randomised controlled trials for ECMO in the
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management of massive pulmonary embolism, single and future studies should help shed light on whether
centre cohort data from an experienced centre sug- ECMO has benefits beyond the current standard of
gest reasonable outcomes (62% overall survival when care and, if so, which patients are likely to derive the
combined with anticoagulation or surgical embolec- greatest benefit. Further technological advances have
tomy, including patients in active cardiac arrest). the potential to greatly alter the current paradigm in
Combining modalities, such as ECMO, thromboly- how we manage patients with severe respiratory and
sis, and catheter directed thrombectomy or embolus cardiac failure.
fragmentation, has also been reported with good out-
comes (70% 30-day survival). Learning Points
Chronic thromboembolic pulmonary hyperten-
• For respiratory failure, ECMO is most commonly
sion may develop as a consequence of recurrent or
used as ‘rescue therapy’ in severe ARDS, in order
unresolved acute pulmonary emboli, the treatment of
to support patients with refractory hypoxaemia.
choice for which remains pulmonary thromboendar-
terectomy (PTE). Residual pulmonary hypertension • Extracorporeal carbon dioxide removal
and reperfusion injury may complicate the post-PTE (ECCO2R) is a version of ECMO in which the
course, both of which may benefit from ECMO sup- primary intention of the device is to remove
port. In cases of isolated reperfusion injury without carbon dioxide from the blood. This technique
haemodynamic compromise, venovenous ECMO may is performed at lower blood flows than are
be sufficient, with earlier institution of ECMO support traditionally required for oxygenation.
associated with better outcomes, though still worse • ECCO2R may facilitate the application of
than outcomes for those who never develop reperfu- standard of care low tidal volume ventilation
sion injury. When PTE is complicated by an inability when respiratory system compliance is reduced.
to wean off cardiopulmonary bypass or residual pul- It may also allow for the use of very low tidal
monary hypertension with right ventricular failure volumes and airway pressures, though more
in the postoperative period, venoarterial ECMO can data are needed before such a strategy can be
offload the right ventricle and support gas exchange recommended. ECCO2R may also have a role
in a similar fashion to other ECMO supported forms in patients with acute hypercapnic respiratory
of pulmonary hypertension, although this is a patient failure, such as acute exacerbations of COPD and
population with a high expected mortality. severe status asthmaticus.
• Recent data suggest that ECMO can
effectively serve as a bridge to either recovery
Future Directions or transplantation in select patients with
Unlike cardiac failure in which destination device decompensated pulmonary hypertension with
therapy exists in the form of ventricular assist devices, right ventricular failure.
there is no destination device therapy for end-stage • In its current form, venovenous ECMO
respiratory failure. Therefore, ECMO for respira- remains a temporary form of support. Ongoing
tory failure in its current form may only serve as a technological advances hold the promise of
bridge to recovery or to lung transplantation. There the development of a destination device that
is hope that as ECMO technology evolves, including would significantly alter the approach to severe,
smaller, more durable circuits with more efficient gas irreversible respiratory failure.
exchange, there will come the development of destina-
tion therapy, effectively an artificial lung. With such
advances, there would be the potential for significant Further Reading
alterations in the way we approach patients with both Abrams D, Bacchetta M, Brodie D. Recirculation in
acute and chronic respiratory failure. venovenous extracorporeal membrane oxygenation.
ASAIO Journal. 2015; 61: 115–121.
Conclusion Abrams DC, Brenner K, Burkart KM, et al. Pilot study of

extracorporeal carbon dioxide removal to facilitate
ECMO has the potential to support a broad spectrum extubation and ambulation in exacerbations of chronic
of diseases that result in severe cardiopulmonary obstructive pulmonary disease. Annals of the American
compromise. Although data remain limited, ongoing Thoracic Society. 2013; 10: 307–314.
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Abrams D, Brodie D. Emerging indications for respiratory failure: life support in the new era. Intensive
extracorporeal membrane oxygenation in adults with Care Medicine. 2012; 38: 210–220.
respiratory failure. Annals of the American Thoracic Mikkelsen ME, Woo YJ, Sager JS, Fuchs BD, Christie JD.
Society. 2013; 10: 371–377. Outcomes using extracorporeal life support for adult
Abrams DC, Brodie D, Rosenzweig EB, et al. Upper-body respiratory failure due to status asthmaticus. ASAIO
extracorporeal membrane oxygenation as a strategy Journal. 2009; 55: 47–52.
in decompensated pulmonary arterial hypertension. Noah MA, Peek GJ, Finney SJ, et al. Referral to an
Pulmonary Circulation. 2013; 3: 432–435. extracorporeal membrane oxygenation center and
Abrams D, Javidfar J, Farrand E, et al. Early mobilization mortality among patients with severe 2009 influenza
of patients receiving extracorporeal membrane A(H1N1). Journal of the American Medical Association.
oxygenation: a retrospective cohort study. Critical 2011; 306: 1659–1668.
Care. 2014; 18: R38. Paden ML, Conrad SA, Rycus PT, Thiagarajan RR;
Berman M, Tsui S, Vuylsteke A, et al. Successful ELSO Registry. Extracorporeal Life Support
extracorporeal membrane oxygenation support Organization Registry Report 2012. ASAIO Journal.
after pulmonary thromboendarterectomy. Annals of 2013; 59: 202–210.
Thoracic Surgery. 2008; 86: 1261–1267. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and
Brodie D, Bacchetta M. Extracorporeal membrane economic assessment of conventional ventilatory
oxygenation for ARDS in adults. New England Journal support versus extracorporeal membrane oxygenation
of Medicine. 2011; 365: 1905–1914. for severe adult respiratory failure (CESAR): a
Chiumello D, Coppola S, Froio S, Colombo A, Del Sorbo multicentre randomised controlled trial. Lancet. 2009;
L. Extracorporeal life support as bridge to lung 374: 1351–1363.
transplantation: a systematic review. Critical Care. The Acute Respiratory Distress Syndrome Network.
2015; 19: 19. Ventilation with lower tidal volumes as compared with
Combes A, Bacchetta M, Brodie D, Muller T, Pellegrino V. traditional tidal volumes for acute lung injury and
Extracorporeal membrane oxygenation for respiratory the acute respiratory distress syndrome. New England
failure in adults. Current Opinion in Critical Care. 2012; Journal of Medicine. 2000; 342: 1301–1308.
18: 99–104. Zapol WM, Snider MT, Hill JD, et al. Extracorporeal
MacLaren G, Combes A, Bartlett RH. Contemporary membrane oxygenation in severe acute respiratory
extracorporeal membrane oxygenation for adult failure. A randomized prospective study. Journal
of the American Medical Association. 1979;
242: 2193–2196.
MCQs
1. Major determinants of systemic oxygenation in 3. Endotracheal extubation in awake patients receiving
venovenous ECMO include all of the following ECMO is:
EXCEPT: (a) Standard of care in all patients
(a) ECMO blood flow rate (b) Standard of care in selected patients
(b) Fraction of delivered oxygen (c) Reasonable but of unproven benefit in selected
(c) Sweep gas flow rate patients
(d) Native lung function (d) Never appropriate
(e) Recirculation 4. Prospective randomised controlled trials have dem-
2. A patient receiving venovenous ECMO develops hypo- onstrated a mortality benefit for which of the follow-
tension in the setting of sepsis. Which of the following ing management strategies in ARDS?
is the most appropriate management option? (a) Low tidal volume ventilation
(a) Increase blood flow rate (b) Prone positioning
(b) Start vasopressors (c) High frequency oscillatory ventilation
(c) Decrease sweep gas flow rate (d) (a) and (b)
(d) Add additional venous drainage cannula (e) (a) and (c)
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5. Venovenous extracorporeal carbon dioxide removal is (c) Severe hypoxaemic respiratory failure
most likely to be effective at managing which of the (d) Acute massive pulmonary embolism
following disease states?
(a) Status asthmaticus
(b) Decompensated pulmonary hypertension
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Section 5 Acute Disorders
Resuscitation after Adult Cardiac

Chapter
25A Surgery
Jonathan H Mackay
Defibrillation, ventilation, pacing and resuscitation basic life support (BLS) guidelines. The traditional
are essential components of cardiac surgical care. The Airway, Breathing, Circulation and Defibrillation
2015 European Resuscitation Council (ERC) guide- (ABCD) algorithm described in previous guide-
lines report the incidence of resuscitation as 0.7–8% lines has been replaced by Circulation, Airway and
after adult cardiac surgery. This wide range is almost Breathing (i.e. CAB). In general, 30 chest compres-
certainly due to resuscitation interventions frequently sions at a rate of 100–120 per minute should now be
being undertaken in house on many cardiac surgical given before any attempt to deliver rescue breaths. The
ICUs, and therefore going under the radar of the clini- efficacy of chest compressions can usually be verified
cal audit. Prompt and effective basic life support (BLS) in the ICU by studying the arterial pressure waveform.
and early defibrillation for shockable rhythms are the Interruptions to chest compressions should be mini-
two most important interventions after cardiac arrest. mised and last less than 10 seconds.
Chest reopening and extracorporeal membrane oxy- In situations where BLS is undertaken, the recom-
genation (ECMO) for patients with refractory car- mended ratio of chest compressions to ventilations is
diogenic shock are additional therapeutic options. now 30:2. More chest compressions and fewer inter-
As patients undergoing cardiac surgery become older ruptions are achieved with this ratio than with the
and sicker, quality of resuscitation will continue to previously recommended 15:2 ratio. In the presence
increase in importance. of a patent airway, effective chest compressions are
considered more important than ventilation in the
Resuscitation Guidelines first few minutes of resuscitation. It should be borne
Conventional basic and advanced life support guide- in mind that coronary perfusion pressure progres-
lines provide a useful framework but require modifica- sively rises during chest compressions and rapidly
tion in the cardiac surgical ICU setting. The European falls with each pause for ventilation. Following a wit-
Association of Cardiothoracic Surgery (EACTS) guide- nessed collapse in a patient with oxygenated arterial
lines summarise the key modifications that must be blood, the initial emphasis should normally be on
considered for adult patients in cardiac arrest after car- chest compressions.
diac surgery. Although current resuscitation algorithms Because chest compressions may be injurious
typically divide arrests into two (shockable and non- immediately following cardiac surgery, external car-
shockable) limbs, EACTS subdivide the non-shockable diac massage is frequently deferred in the cardiac ICU
category and utilise a three-limb approach. The EACTS providing defibrillation or external pacing therapy
three-limb model emphasises important initial differ- can be delivered within 30–60 seconds. The rationale
ences in management of patients presenting with severe for this approach and modifications to the Advanced
bradycardia or asystole compared to those presenting Life Support (ALS) algorithm are discussed later.
with pulseless electrical activity (see Figure 25A.1).
Important changes in the revised 2015 European Adult Advanced Life Support
Resuscitation Council guidelines are discussed below. The new 2015 Advanced Life Support (ALS) algo-
rithm for the management of cardiac arrest in adults
Adult Basic Life Support retains the shockable and non- shockable limbs
Maintaining the circulation has been promoted ahead (Figure 25A.2). There are subtle but important dif-
of airway management and breathing in recent adult ferences in recommendations for defibrillation for
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Section 5: Acute Disorders
Figure 25A.1 EACTS guideline for resuscitation of a

CARDIAC ARREST postoperative cardiac surgical ICU (or recovery) patient.
From Dunning et al. (2009).
Assess rhythm
Ventricular Asystole or Pulseless

fibrillation or severe electrical
tachycardia bradycardia activity
DC shock Pace
(3 attempts) (if wires
available)
Start basic life support
Amiodarone Atropine 3 mg If paced, turn

300 mg consider off pacing to
via central external exclude
venous line pacing underlying VF
Prepare for emergency resternotomy
Continue CPR with

Continue CPR Continue CPR
single DC shock
until until
every 2 minutes until
resternotomy resternotomy
resternotomy
Airway and ventilation

• If ventilated turn FiO2 to 100% and switch off PEEP.
• Change to bag/valve with 100% O2, verify ET tube position and cuff inflation
and listen for breath sounds bilaterally to exclude a pneumothorax or haemothorax.
• If tension pneumothorax suspected, immediately place large bore cannula in the
2nd rib space anterior mid-clavicular line.
DO NOT GIVE ADRENALINE unless a senior doctor advises this.
If an IABP is in place change to pressure trigger.
Do not delay basic life support for defibrillation or pacing for more than 1 minute.
shockable rhythms in cardiothoracic ICU and the Since 2005, a single shock (>150 J biphasic or 360 J
catheter laboratory. The EACTS guidelines include monophasic) has been recommended instead of three
important advice on how to expedite the decision ‘stacked’ shocks, in general hospitals. Interruptions to
making and actual chest reopening process (see CPR during delivery of three shocks and improved
Figure 25A.1). first shock efficacy of biphasic defibrillators were cited
as reasons for the change. In practice, most cardiac
Pulseless VT/VF surgical ICU and catheter laboratory staff were uncon-
Pulseless VT and VF account for the majority of vinced by the evidence for single shocks and contin-
underlying dysrhythmias in patients who survive car- ued to deliver up to three stacked shocks in quick
diac arrest in hospitals. For every minute the chances succession when treating VF. More recent EACTS and
of successful defibrillation decline by 7–10%. Specialist ERC guidelines recognised this and recommend three
cardiothoracic units should be capable of early detec- stacked shocks in quick succession for VF/VT arrests
tion, rapid defibrillation and superior outcomes. In occurring in the cardiac catheter laboratory and car-
the setting of the cardiac ICU, when external cardiac diac surgical ICU. In addition, contrary to the latest
massage may be injurious, immediate defibrillation guidelines, there is usually no need to commence
(i.e. DCAB) should be the first line response for all chest compressions after a successful shock in inva-
monitored in-hospital VF arrests. sively monitored cardiac surgical patients.
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Chapter 25A: Resuscitation after Adult Cardiac Surgery
Table 25A.1 An aide memoire to the causes of pulseless Suggested modifications to the standard ALS algo-
electrical activity and asystole rithm are shown in Figure 25A.2.
The Four ‘Hs’ The Five ‘Ts’
Hypoxia Tension pneumothorax Drugs in Advanced Cardiac
Hypovolaemia
Hyperkalaemia
Tamponade
Thromboembolic
Life Support
Hypothermia Therapeutic substances in overdose
Although the use of vasopressors at cardiac arrests
Toxic substances has become standard practice, proof of efficacy is
limited. Epinephrine 1 mg is recommended every 3
minutes to improve coronary and cerebral perfusion.
Non-VF/VT Arrests The American Heart Association has suggested that
vasopressin may be used as an alternative to epineph-
A heterogeneous group of conditions may present as
rine. Clinical studies, however, have failed to demon-
non-VF/VT cardiac arrest (Table 25A.1). Outcome is
strate that either vasopressin or high dose epinephrine
generally poor unless a reversible cause can be found
(5 mg) offers any additional benefit.
and treated effectively. In the cardiac surgical ICU –
On the cardiac surgical ICU it is entirely appro-
where bleeding, hypovolaemia and tamponade are all
priate to modify the recommended pharmacologi-
readily treatable, and where additional therapeutic
cal management of a monitored cardiac arrest. An
options are available –outcomes are considerably bet-
α-agonist or smaller initial dosages of epinephrine
ter than in the general ICU population. Examination
(0.1–0.2 mg) may be administered to minimise the
of trends in RA pressure, PAWP and airway pressure
risk of hypertension and tachycardia following suc-
all provide useful pointers as to the likely aetiology.
cessful resuscitation. For patients with VF/VT arrests,
Cessation of drainage from mediastinal drains does
it is standard practice to attempt at least three shocks
not exclude haemorrhage or tamponade as the drains
before giving any epinephrine.
may have become blocked. Although TTE and TEE
The evidence supporting the use of antiarrhythmic
echocardiography is often very useful in the cardiac
drugs in VF/VT is surprisingly weak. Two studies of
ICU, echocardiography may miss localised collections
out-of-hospital VF/VT arrest demonstrated that the
and thus delay reoperation. Patients with clinical signs
administration of amiodarone after three unsuccessful
suggestive of tamponade should be reopened even if
shocks increased the likelihood of survival to hospital
echocardiography is inconclusive.
admission. Significantly, neither study demonstrated
When faced with an arrest of this type, it is
that amiodarone improved survival to discharge.
essential to:
Despite this latter finding, amiodarone has now been
• confirm that VF is not being missed and that promoted ahead of lidocaine in the pulseless VF/VT
ECG leads or pads are correctly attached, algorithm. A bolus of amiodarone 300 mg is recom-
• treat bradycardia with epicardial pacing if wires mended for VF/VT arrests that persist after three
are present, shocks but this should not delay surgical reopening
• exclude tension pneumothorax, (see below). A further dose (150 mg) may be given for
• exclude underlying VF in the presence of fixed recurrent or refractory VF/VT, followed by an infu-
rate pacing, and sion of 900 mg over 24 hours. Lidocaine can still be
• consider chest reopening if closed chest CPR is given for VF/VT if the patient has received amiodar-
unsuccessful. one but the evidence supporting its efficacy is weak.
Symptomatic bradycardia is extremely common in the Magnesium should also be considered if there is clini-
cardiac surgical ICU. ALS guidelines no longer recom- cal suspicion of hypomagnesaemia. Administration of
mend atropine as first line treatment. In the cardiac sodium bicarbonate should be considered if arterial or
surgical ICU, where tachycardia is equally undesir- mixed venous pH < 7.1.
able, pacing (when possible) is the preferred option. If
pacing is not an option (e.g. no wires in situ or failure Airway and Ventilation
to capture), isoproterenol or dopamine are often used. The Fourth National Audit Project (NAP4) of the
Management of asystole that fails to respond to pacing Royal College of Anaesthetists reported that 61%
is an indication for prompt chest reopening. (22 of 36) of airway events in the ICU led to death or
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Unresponsive?
Open airway
Look for signs of life
Call
Resuscitation Team
CPR 30:2
Until defibrillator/monitor
attached
Assess
rhythm
Immediate
Shockable Treat bradycardias
defibrillation Non-shockable with epicardial pacing
BEFORE cardiac (VF/pulseless VT) (PEA/asystole)
if wires in situ
massage
During CPR:
Correct reversible causes* Exclude
Check electrode position underlying VF in
Three 1 Shock and contact the presence of
shocks 150–360 J biphasic Attempt / verify: fixed-rate pacing
or 360 J monophasic IV access
airway and oxygen
Give uninterrupted
compressions when
airway secure
Immediately resume Give adrenaline
every 3–5 min
* Immediately resume
CPR 30:2 Consider: amiodarone,
CPR 30:2
for 2 min atropine, magnesium for 2 min
*Reversible causes
Hypoxia Tension pneumothorax
Hypovolaemia Tamponade, cardiac
Hypo/hyperkalaemia/metabolic Toxins
Hypothermia Thrombosis (coronary or pulmonary)
*Reduce initial dose of adrenaline from 1.0 mg to 0.1–0.5 mg
Consider chest re-opening after two cycles of resuscitation
Figure 25A.2 Algorithm for resuscitation after adult cardiac surgery. Six suggested modifications to the standard ALS algorithm are
highlighted in the six bright yellow boxes to the sides and below. Therapeutic hypothermia may be considered after successful resuscitation.
Adapted from the Resuscitation Council (UK) 2010 ALS algorithm. (A black and white version of this figure will appear in some formats. For
the colour version, please refer to the plate section.)
persistent neurological injury. Major risk factors for tube position and patency, and ventilation, capnogra-
adverse events included anaesthetic experience of phy also provides invaluable additional information
doctors, out-of-
hours airway interventions, patient about return of spontaneous circulation and cardiac
obesity and failure to use (or correctly interpret) cap- output (see Table 25A.2). The introduction of manda-
nography. A recurrent finding was the failure to con- tory waveform capnography in the CICU has argu-
sider the possibility of oesophageal intubation when ably made the single biggest contribution to improved
presented with a flat capnograph trace. As well as patient safety on the CICU since the publication of the
providing valuable information about endotracheal first edition of CTiCICU 1e nearly a decade ago.
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Table 25A.2 Waveform capnography during ALS resuscitation of a patient who would otherwise die.
Confirmation of tracheal intubation Hypothermic CPB restores organ perfusion, decom-
Monitoring ventilation rate
presses the heart, and allows the surgeon to consider
all possible options in a more controlled setting. Valve
Monitoring quality chest compressions
replacement, repair of bleeding cannulation sites, graft
Identifying ROSC during CPR
revision and additional grafting may be undertaken
Prognostication during CPR: failure to achieve CO2 value >1.33 with often surprisingly successful clinical outcomes.
kPa (10 mmHg) after 20 minutes CPR associated with poor
outcome
Whenever possible the patient should be transferred
to the operating room before emergency reinstitution
of CPB.
Chest Reopening VA ECMO is a therapeutic option for those who
Following surgery through a sternotomy, chest reo- cannot be weaned from emergency bypass. The indi-
pening is both a diagnostic and therapeutic option in cations, methods and outcomes of postcardiotomy
the cardiac surgical ICU. In addition, chest reopening ECMO are discussed elsewhere.
allows internal cardiac massage, which is consider-
ably more effective than external chest compressions. Late Resuscitation on the ICU
Haemorrhage, tamponade, graft occlusion and graft Patients with greater preoperative surgical risk,
avulsion are conditions likely to be remedied by this adverse intraoperative events and poor physiologi-
approach. Patients most likely to benefit are: those cal state at the time of ICU admission are less likely
with a surgically remediable lesion, those who arrest to survive to hospital discharge. Similarly, refractory
within 24 hours of surgery and those in whom the multisystem organ failure and recurrent nosocomial
chest is reopened within 10 minutes of arrest. Delayed infection have been shown to be important determi-
reopening or the finding of a problem that is not ame- nants of mortality. For some patients, there comes a
nable to surgery (e.g. global cardiac dysfunction) is point when aggressive resuscitation is inappropri-
associated with a poor prognosis. Recent resuscita- ate and cardiopulmonary arrest becomes a termi-
tion guidelines confirm that chest reopening should nal event. It is the duty of a doctor to identify these
be triggered by: patients and to ensure that they are spared the indig-
• three failed shocks in VF/VT arrests (i.e. one nity of futile interventions.
resuscitation cycle); DNAR directives should be instituted if it is
• exclusion of reversible causes (e.g. tension believed that death is inevitable and that CPR is
pneumothorax) and failure of initial treatment for unlikely to be successful. Sensible guidelines on
non-VF/VT arrest. implementation of DNAR orders can be found on the
Chest reopening should not be used as a ‘last ditch’ UK Resuscitation Council’s website (www.resus.org.
manoeuvre after a prolonged period of unsuccessful uk/dnacpr).
resuscitation. Although some units advocate initially
stopping all infusions and syringe drivers to exclude Resuscitation Outside the ICU
iatrogenic drug administration errors, the majority
tend to continue infusions unless there is a clinical General Ward or Surgical Floor
suspicion of inadvertent vasodilator flushing being The management of a cardiac arrest outside the ICU
responsible for loss of CO. Whichever policy is used, differs little from a cardiac arrest on a general surgi-
it is important to ensure that anaesthesia and analge- cal or medical ward. Seemingly trivial symptoms and
sia are restored prior to chest reopening. The EACTS vague ‘early warning’ signs should be taken seriously
guidelines and Cardiac Advanced Life Support (CALS) as they may herald a more sinister event. Although
courses recommend six key roles in the management some arrests are unheralded, the majority of patients
of a cardiac surgical ICU arrest (Figure 25A.3). who arrest in the general ward setting display signs of
physiological deterioration long before the event.
Cardiopulmonary Bypass and ECMO Early intervention seems intuitive and may reduce
The reinstitution of cardiopulmonary bypass (CPB) the incidence of cardiac arrests in the surgical ward
following emergency chest reopening may allow the setting. Early warning scores (EWS) are used to ‘track’
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216
Syringe Ventilator
Drivers
5
2 Defibrillator
Patient
1
3
Sternotomy
Trolley
Six key roles in the cardiac arrest:

1. External cardiac massage
2. Airway and breathing
3. Defibrillation
4. Team leader
5. Drugs and syringe drivers
6. ICU co-ordinator
Figure 25A.3 Six key roles in cardiac surgical ICU arrest. From Dunning et al. (2009).
patients’ physiological status and ‘trigger’ a response mortality from unexpected ward arrests in general
or intervention. Tracking the patient –the so-called hospitals. The effectiveness of the MET concept is sig-
‘afferent limb’ –involves either a single or multiple nificantly hampered by incomplete documentation of
parameter scoring system. Single parameter scoring patient observations. Given the importance of respira-
systems have limitations. Many of the suggested crite- tory rate and urinary output, recording of these values
ria for triggering a response are actually relatively late is often surprisingly poor.
markers of physiological deterioration (Table 25A.3). The relative success of chest reopening following
Aggregated weighted systems may provide earlier cardiac arrest on the ICU cannot be reproduced when
warning of deterioration and can be adapted for use chest reopening is undertaken on the ward or surgical
in cardiothoracic wards (Table 25A.4). floor. The proportion of surgically remediable causes
The use of medical emergency teams (MET) has of cardiac arrest decreases exponentially after surgery.
been shown to reduce both the incidence of and As time passes, thromboembolic phenomena and
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217
cardiac failure become more common than surgical decision to reopen on the cardiac ICU. Whereas there
bleeding or tamponade. A small number of patients is level-one evidence to support chest reopening in the
who sustain a witnessed arrest on the ward or surgical cardiac ICU, the latest ERC guidelines do not specifi-
floor may benefit from chest reopening either locally cally address the role of chest reopening for patients
with appropriate facilities or in the operating room. who arrest outside the cardiac ICU. A scoop and run
The decision to reopen a ward patient either locally or approach should be considered following:
after ‘scoop and run’ is usually more difficult than the 1. A witnessed arrest;
2. Unexpected arrest in a patient who had initially
Table 25A.3 Suggested criteria for calling the medical been making good progress;
emergency team in a cardiothoracic hospital; oximetry
is widely available and a potentially useful monitor in a
3. Tension pneumothorax considered and excluded;
cardiothoracic ward 4. Close proximity to operating theatres;
5. Non-VF/VT arrest with a high index of suspicion
Acute change Physiology
of hypovolaemia (major bleeding), tamponade,
Airway Threatened acute thromboembolism or air embolism;
Breathing All respiratory arrests 6. VF/VT arrests unresponsive to DC shocks that
Respiratory rate <5 or >36 may have acute graft occlusion.
Circulation All cardiac arrests
A patient’s suitability for chest reopening and reinsti-
Pulse rate <40 or >140
tution of CPB should be considered after one cycle of
Neurology Fall in Glasgow coma scale (GCS) score >2
CPR. The decision to scoop and run must be made
points
early because time is of the essence. Good quality chest
Renal Urine output <0.5 ml/kg/hr for 2
compressions and ventilation must be maintained
consecutive hours
during transfer. Epinephrine 1 mg (or an alternative
Oximetry SpO2 < 90% regardless of FiO2
vasopressor) should be given every 3–5 minutes as
Other Patients giving cause for concern who do
per standard ALS guidelines, rather than the reduced
not meet above criteria
dosages recommended in cardiac surgical ICU for
Table 25A.4 Papworth Cardiothoracic Early Warning Score (CTEWS)
Score Tem Neuro Respiratory pO2/ Heart Systolic BP Urine output

p( 0C) AVPU or rate FiO2ratio rate catheter in situ
ACDU No catheter
3 ≤35.0 Unresponsive ≤8 <18 <40 ≤75 <0.1 ml/kg/hr
2 35.1–35.5 Response 9–10 18–24.9 40–44 76–85 ≥0.1 ml/kg/hr
to pain <0.3 ml/kg/hr
1 35.6–36.0 Response 25–34.9 45–50 86–100 ≥0.3 ml/kg/hr
to voice <0.5 ml/kg/hr
0 36.1–38.0 Alert 11–19 ≥35 51–104 101–199 ≥0.5 ml/kg/hr
or PU
<6 hr – day
<10 hr –night
1 38.1-38.4 Confused 20–24 105–134 NPU
≥6 hr day
≥ 10 hr night
2 ≥38.5 Drowsy 25–29 ≥135 ≥200 NPU
≥ 12 hr
3 Unresponsive ≥30 NPU
≥ 18 hr
** pO2/FiO2 ratio = (kPa).
PU = passed urine; NPU = not passed urine.
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patients in the immediate postoperative period. It

needs to be emphasised that scoop and run will only
Learning Points
be successful if both the heart and brain are success- • ALS algorithms require modification in the
fully restored to normal or near-normal function. cardiac surgical ICU.
• Consider the possibility of underlying VF
in ‘asystolic’ arrests and paced patients with
Catheter Laboratory Arrests apparent pulseless electrical activity.
VF/VT arrests during elective procedures in the cathe- • Look for epicardial pacing wires in bradycardic
ter laboratory are invariably iatrogenic, typically ame- arrests before giving atropine and epinephrine!
nable to very early defibrillation and associated with
• The majority of cardiac arrests after cardiac
return of spontaneous circulation in >90% of cases,
surgery are heralded by symptoms and signs.
and have >80% chance of survival to discharge. As
discussed earlier, recent ERC guidelines recommend
administration of three stacked shocks in quick suc-
cession for VF/VT arrests occurring in the cardiac
Further Reading
catheter laboratory. In cases of coronary dissection or Cook TM, Woodall N, Harper J, Benger J; Fourth National
other surgically amenable conditions, early considera- Audit Project. Major complications of airway
tion of transfer to the operating room and institution management in the UK: results of the Fourth National
Audit Project of the Royal College of Anaesthetists and
of CPB should be considered. the Difficult Airway Society. Part 2: intensive care and
Patients undergoing primary percutaneous inter- emergency departments. British Journal of Anaesthesia.
vention who require airway intervention present similar 2011; 106: 632–642.
challenges to those on the ICU albeit in a remote envi- Dunning J, Fabbri A, Kolh PH, et al. Guideline for
ronment with potentially limited immediate anaesthetic resuscitation in cardiac arrest after cardiac surgery.
support. As with the ICU, skilled anaesthetic assistance European Journal of Cardio-Thoracic Surgery. 2009;
and waveform capnography are both mandatory. 36: 3–28.
ECMO assisted CPR, so-called E-CPR, is an addi- Mackay JH, Powell SJ, Osgathorp J, Rozario CJ. Six-year
tional therapeutic option for selected patients in ECMO prospective audit of chest reopening after cardiac
centres. The CHEER trial recently reported that 14 of arrest. European Journal of Cardio-Thoracic Surgery.
26 (54%) patients with refractory in-hospital and out- 2002; 22: 421–425.
of-hospital arrests survived to hospital discharge with Nielsen N, Wetterslev J, Cronberg T, et al. Targeted
full neurological recovery. Running a 24/7 catheter temperature management at 33°C versus 36°C after
laboratory ECMO service mandates funding of: cardiac arrest. New England Journal of Medicine. 2013;
369: 2197–2206.
1. Resident (or very close proximity) consultant
Sandroni C, Cariou A, Cavallaro F, et al. Prognostication
cardiologist, intensivist and perfusion cover;
in comatose survivors of cardiac arrest: an advisory
2. ICU costs associated with potentially prolonged statement from the European Resuscitation
ICU lengths of stay awaiting neurological Council and the European Society of Intensive
prognostication in comatose survivors. Care Medicine. Intensive Care Medicine. 2014;
40: 1816–1831.
Conclusion Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac

arrest treated with mechanical CPR, hypothermia,
Patients sustaining cardiac arrests in a cardiothoracic ECMO and early reperfusion (the CHEER trial).
surgical unit are twice as likely to survive to hospital Resuscitation. 2015; 86: 88–94.
discharge as patients who arrest in a general hospi- Truhlar A, Deakin C, Soar J, et al. European Resuscitation
tal. The essential requirements for a good clinical Council Guidelines for Resuscitation 2015
outcome are early detection, effective BLS and early Section 4. Cardiac arrest in special circumstances.
defibrillation. Resuscitation. 2015; 95: 148–201.
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MCQs
1. Aetiology of arrests in the cardiac surgical ICU: (c) Can be undertaken by any member of the team
(a) Vast majority unheralded (d) Is usually associated with poor outcomes
(b) Commonly due to mild hypothermia (temperature (e) Is no longer necessary due to advances in
34.0–35.0 oC) AV ECMO
(c) Commonly due to moderate hyperkalaemia (K+ 4. PEA arrests due to tamponade:
5.5–6.0) (a) Are usually unheralded
(d) Almost invariably due to unstable arrhythmias (b) External massage may be ineffective
(e) Bleeding is the most common cause (c) A focused TTE is mandatory within 5 minutes
2. VF arrests in the cardiac surgical ICU: of arrest
(a) Immediate BLS 30:2 always (d) TTE has >90% sensitivity, >90% specificity
(b) Prepare to restart chest compressions after (e) Can usually be managed by needle paracentesis
single shock 5. Capnography in the cardiac ICU:
(c) Amiodarone (300 mg) and adrenaline (1 mg) (a) Rarely provides useful information
should be given within 3 minutes of arrest
(b) Is desirable in spontaneously breathing patients
(d) May be due to problems with intracardiac air or
graft malfunction (c) High ETCO2 is a hallmark of deteriorating cardiac
function
(e) Chest compressions are required after successful
shock to reduce LV distension (d) Is mandatory in all cardiac arrests requiring airway
intervention
3. Chest reopening in the cardiac surgical ICU:
(e) Failure to achieve CO2 value >4 kPa (40 mmHg)
(a) Should only be undertaken by a surgeon after 20 minutes CPR is associated with a poor
(b) Should only be undertaken as a last resort outcome
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Out-of-Hospital Cardiac Arrest Patients

Chapter
25B in the Cardiothoracic Intensive Care Unit

Lisen Hockings and Sophia Fisher
Introduction • early defibrillation to restart the heart;

• post-resuscitation care to restore quality of life.
Patients suffering from cardiac arrest in the commu-
nity and surviving it are frequently transferred to a
ILCOR publishes a five yearly update to the
cardiothoracic centre where further investigations
International Consensus on cardiopulmonary resus-
and treatment are possible. The majority of these
citation (CPR) and emergency cardiovascular care
patients have already been intubated and ventilated,
(ECC) Science with Treatment Recommendations
and are transferred directly to an angiography labo-
(CoSTR). This document forms the basis for guide-
ratory where percutaneous interventions are per-
lines that are subsequently produced and endorsed
formed. Once the investigations and treatment in the
by member organisations. An in-depth discussion of
angiography laboratory are completed the patients are
basic and advanced life support is beyond the scope
then transferred to the cardiothoracic intensive care
of this chapter.
unit for further management.
Strategies that have led to increased survival in a
With the advent and increasing availability of
variety of settings have included systematic commu-
mechanical circulatory support (MCS) devices
nity based projects to enhance first responder CPR
(including mechanical chest compression devices
training, increased numbers of public access auto-
(MCCD) and extracorporeal membrane oxygenation
mated external defibrillators (AEDs) and protocolised
(ECMO)/extracorporeal CPR (ECPR)) there are likely
in-hospital care pathways.
to be increasing numbers of out-of-hospital cardiac
arrest patients transported to hospitals whilst still in
cardiac arrest. Critical care clinicians must be com-
fortable with continuing high quality CPR and ACLS
The Post-cardiac Arrest Syndrome
and with the operation of MCS devices. Overall survival and long-term outcomes after OHCA
are related to the underlying cause of the arrest, the
hypoxaemic/ischaemic insult to the brain and other
Survival organs during the period of circulatory arrest, and
Survival after out-of-hospital cardiac arrest (OHCA) to the severity of the post-cardiac arrest syndrome
is increasing but remains low, and varies across geo- (PCAS) that occurs with reperfusion –in the setting
graphic regions and institutions. Where outcomes have of a return of spontaneous circulation (ROSC) or with
improved it appears to be in younger patients and in institution of MCS.
those who have an initial shockable rhythm. This has Post-
cardiac arrest care begins immediately on
been attributed to a focused improvement in each of reinstitution of circulation. Some patients with a read-
basic life support (BLS), advanced cardiac life support ily reversible cause and short duration of cardiac arrest
(ACLS) and post-resuscitation care (PRC) –the ele- will suffer very little, if any, systemic insult. Immediate
ments that form a continuum of links in the ‘chain of goals of treatment having achieved restoration of cir-
survival’ (Figure 25B.1) outlined by the International culation (ROSC or MCS) include the diagnosis and
Liaison Committee on Resuscitation (ILCOR): management of the underlying cause of the cardiac
• early recognition and call for help to prevent arrest in order to prevent recurrence, minimising
cardiac arrest; ongoing injury from both the cardiac arrest itself
• early cardiopulmonary resuscitation (CPR) to buy and the insults from reperfusion injury, and multiple
time; organ support.
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Chapter 25B: Out-of-Hospital Cardiac Arrest Patients
ition
and ca uscitation c
gn
ll fo t res ar
co r os
e
P
re
he
Early CPR brillation
Defi
lp
y
Earl
ly
ar
E
- to p
life
of
re
en
it y
v
tc -t al
ardia st o re
store qu
c arre
-t rt
-t or
ob
u y ti m e estar th e hea
t
Figure 25B.1 Chain of survival, courtesy of the Adult Basic Life Support Guidelines of the Resuscitation Council. (A black and white version
of this figure will appear in some formats. For the colour version, please refer to the plate section.)
Four key components of PCAS have been described: cardiovascular instability, complications from sys-
• Post-cardiac arrest brain injury; temic ischaemia-reperfusion (hypo/hypergycaemia,
• Post-cardiac arrest myocardial dysfunction; hyperthermia), and persistent precipitating pathology
(hypoxaemia)) as well as potentially by therapeutic
• Systemic ischaemia/reperfusion response;
interventions (hypo/hypercarbia, hyperoxia).
• Persistent precipitating pathology.
Post-cardiac Arrest Brain Injury Post-cardiac Arrest Myocardial

The brain is particularly vulnerable to hypoxic Dysfunction
ischaemic injury in the setting of circulatory arrest. Haemodynamics in the immediate post-ROSC setting
Reperfusion is associated with an ongoing cascade of can be extremely labile, reflecting circulating endoge-
cerebral injury. Mechanisms are incompletely under- nous and exogenous catecholamines, and an ischaemia-
stood but are thought to include: disruptions to calcium reperfusion injury to the myocardium (regardless of
homeostasis, excitotoxicity, alterations in membrane the initial cause of arrest). Following cardiac arrest
permeability with resultant cellular oedema, free there is a period of myocardial ‘stunning’ that occurs
radical generation, mitochondrial dysfunction and despite evidence of preserved coronary blood flow
activation of apoptotic pathways. Cerebrovascular (where coronary ischaemia was not the primary cause
autoregulation may be impaired for an extended of cardiac arrest) characterised by global hypokinesis
period of time following cardiac arrest. and elevated filling pressures. Observational data and
Clinical findings in post-cardiac arrest brain injury animal studies suggest that this reversible period of
include coma, seizures, myoclonus, neurocognitive myocardial stunning lasts for up to 72 hours.
dysfunction and in the most severe cases, brain death. Clinically this can manifest as dysrhythmia, hypo-
Post-cardiac arrest brain injury is the leading cause of tension and evidence of a low cardiac output state with
morbidity and mortality after cardiac arrest. The pro- systemic hypoperfusion. Treatment is supportive and
tracted pattern of neuronal cell death suggests a wide can include judicious fluid administration, inotropes,
therapeutic window with multiple potential phar- vasopressors, temporary pacing and MCS (intra-aor-
macological and physiological interventions to opti- tic balloon counterpulsation pump (IABP), venoarte-
mise outcome. To date, only therapeutic temperature rial ECMO or left ventricular assist device (LVAD)).
management has shown any likelihood of improved Cardiovascular instability and complications remain a
outcomes. Post- cardiac arrest brain injury may be leading cause of death in patients who survive an ini-
compounded by the other features of PCAS (persistent tial cardiac arrest.
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Systemic Ischaemia-Reperfusion • Hypoxia

• Hypovolaemia
Response • Hypokalaemia/hyperkalaemia/other metabolic
Circulatory arrest prevents tissue oxygen and nutri- • Hypothermia/hyperthermia
ent delivery and metabolic waste removal. Even with • Thrombosis –coronary or pulmonary
continuous CPR there is an accumulated systemic
• Tension pneumothorax
oxygen debt that causes endothelial activation and
• Tamponade – cardiac
cellular (and subsequently organ) dysfunction and
results in generalised activation of the inflammatory • Toxins
and coagulation cascades. The endothelial glycoca- Assessment of likely antecedent cause(s) for the car-
lyx appears to play a central role in these processes. diac arrest must occur contemporaneously with ACLS
Systemic hypoperfusion may self- propagate and and post-resuscitation care. This involves collateral
progress even with reinstitution of circulation due history from first responders, paramedics, family
to postcardiac arrest myocardial dysfunction, members and medical staff as well as a focused clini-
vasodilatation and microcirculatory failure. This cal examination and investigations where appropriate.
‘systemic inflammatory response syndrome’ (SIRS) Persistent precipitating pathology can both con-
shares many features with sepsis and can result in found and complicate management of the post-
the clinical appearance of relative hypovolaemia cardiac arrest patient. Asphyxiation is associated with
(with interstitial oedema and capillary leak), abnor- more severe cerebral oedema and post-cardiac arrest
mal circulatory autoregulation, impaired oxygen brain injury than other causes of circulatory arrest.
delivery and uptake, and an increased susceptibil- A SIRS response in the setting of sepsis may potenti-
ity to infection. The severity of the syndrome and ate the haemodynamic instability and multiple organ
markers of inflammation are associated with a dysfunction associated with systemic ischaemia-
poorer prognosis. reperfusion. Acute coronary syndrome (ACS) as a
cause for cardiac arrest will exacerbate post-arrest
Persistent Precipitating Pathology myocardial dysfunction, and early percutaneous coro-
Primary myocardial disease is the most common nary intervention has been associated with improved
cause of OHCA. However, circulatory arrest can be neurologically intact survival.
the presenting feature or final common pathway in
any number (if not all) pathologies. More common
Intensive Care Management
etiologies can include the following: The intensive care management of OHCA patients
involves the diagnosis and treatment of the underly-
Respiratory pulmonary embolus; pneumothorax; ing cause for the arrest, managing subsequent cardio-
hypoxaemia –drowning, aspiration,
vascular dysfunction, minimising and managing any
asphyxiation; end-stage chronic obstruc-
tive airways disease (COAD), asthma
further organ damage, and prognostication. Critical
care physicians are increasingly involved in the very
Neurological subarachnoid haemorrhage (SAH), cer-
ebrovascular accident, prolonged seizures
early management of cardiac arrest patients –as part
of rapid response teams (RRTs) attending in-hospital
Sepsis
cardiac arrest (IHCA) and as an integral part of proto-
Metabolic including electrolyte abnormalities and colised in-hospital care pathways for OHCA patients.
temperature derangement Due to a relative paucity of high quality research in
Trauma hypovolaemia (haemorrhage), tension post-resuscitative care, there are only limited data to
pneumothorax, tamponade support specific interventions. However, several hos-
Toxicology envenomation and overdoses pital level critical care interventions have consistently
Where cardiac arrest has occurred as a result of a been associated with improved outcomes after OHCA
systemic illness, the likelihood of sustained ROSC (see Figure 25B.2):
when the underlying pathology has not been treated • Early percutaneous coronary intervention (PCI);
is remote. Addressing potentially reversible causes • Targeted temperature management (TTM);
remains a key component of ACLS resuscitation algo- • Delayed prognostication before withdrawal of
rithms with the 4 Hs and 4 Ts mnemonic: cardiorespiratory supports.
14:45:53
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Return of spontaneous circulation and comatose
Airway and breathing

Maintain SpO2 94 – 98%
Insert advanced airway
Waveform capnography
Immediate treatment
Ventilate lungs to normocapnia
Circulation
12-lead ECG
Obtain reliable intravenous access
Aim for SBP > 100 mmHg
Fluid (crystalloid) – restore normovolaemia
Intra-arterial blood pressure monitoring
Consider vasopressor/inotrope to maintain SBP
Control temperature
Constant temperature 32°C – 36°C
Sedation; control shivering
NO Likely cardiac cause? YES
YES 12-lead ECG ST elevation?

Diagnosis
NO
Consider
Coronary angiography ± PCI
coronary angiography ± PCI
NO
Consider CT brain Cause for cardiac arrest
and/or CTPA identified?
YES
Treat non-cardiac cause of

Admit to Intensive Care Unit
cardiac arrest
ICU management
Temperature control: constant temperature 32°C – 36°C
for ≥ 24h; prevent fever for at least 72 h
Maintain normoxia and normocapnia; protective ventilation
Optimise haemodynamics
Optimising recovery
(MAP, lactate, ScvO2, CO/Cl, urine output)

Echocardiography
Maintain normoglycaemia
Diagnose/treat seizures (EEG, sedation, anticonvulsants)
Delay prognostication for at least 72 h
Secondary prevention
Follow-up and
e.g. ICD, screen for inherited disorders,
rehabilitation
risk factor management
Figure 25B.2 Post-resuscitation care algorithm. SBP systolic blood pressure; PCI percutaneous coronary intervention; CTPA computerised
tomography pulmonary angiogram; ICU intensive care unit; MAP mean arterial pressure; ScvO2 central venous oxygenation; CO/CI cardiac
output/cardiac index; EEG electroencephalography; ICD implanted cardioverter defibrillator.
Image courtesy of Elsevier Limited.
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A Practical Approach Computerised tomography (CT) brain/chest: may

reveal intracranial haemorrhage as the cause
Assessment and management of the post-ROSC OHCA
of the arrest, or cerebral oedema as a result of
patient should occur simultaneously, using a team-based
ischaemic-hypoxic injury. In selected patients a
approach with an initial focus on the airway, breathing
CT chest scan may reveal a pulmonary embolus
and circulation. History, examination, investigations
or aortic pathology.
and treatment should occur contemporaneously.
In the unconscious patient collateral history must Treatment algorithms should include general
be obtained from first responders, paramedic and management of the OHCA patient and specific inter-
emergency staff, medical records, and family members. ventions depending on the cause of the arrest.
Physical examination should focus on excluding
persistent precipitating pathologies and an assessment
of the adequacy of circulation and end-organ perfusion. Early Percutaneous Coronary
Important investigations to aid diagnosis and Intervention (PCI)
subsequent management include the following: In patients where there is not an obvious non-cardiac
12-lead electrocardiogram (ECG): to identify evidence cause of arrest, early PCI is associated with improved
of coronary ischaemia, abnormal conduction such overall survival, and improved neurological out-
as a prolonged QT interval, or right heart strain comes. This includes patients without obvious ST seg-
(suggestive of a pulmonary embolus). ment elevation myocardial infarction (STEMI).
Transthoracic echocardiography (TTE): ultrasound However, routine PCI in OHCA involves signifi-
is playing an increasing role in emergency and cant resource utilisation and further randomised con-
critical care medicine and is now incorporated trolled trials are required to clearly define the optimum
into ALS algorithms. Early focused and/or formal timing and role for PCI in this cohort (Table 25B.1).
TTE may help to differentiate the aetiology of
OHCA and guide treatment decisions.
Blood tests: these include a full blood count, a blood Haemodynamics
group and screen, electrolytes, urea and creatinine, Invasive arterial monitoring is recommended for con-
troponin, and early arterial blood gas to help tinuous assessment of blood pressure, titration of flu-
establish the cause of the arrest, assess the severity ids/vasoactive agents and to facilitate blood sampling.
of insults and provide baseline information. Large bore peripheral access may be used for fluid
Toxicology analysis may be considered. administration to correct any hypovolaemia. Where
Chest X-ray: evaluation of primary pulmonary vasoactive agents (inotropes/vasopressors) are being
pathology, potential injuries sustained during considered, a central venous line should be inserted.
resuscitation and the correct position of an There is no evidence that defines an optimal target
endotracheal tube and central vascular access. for mean arterial pressure (MAP). The aim should be to
Table 25B.1 Percutaneous coronary intervention

Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are
comatose after OHCA of suspected cardiac origin with ST elevation on ECGb
Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are
comatose after OHCA of suspected cardiac origin but without ST elevation on ECGd
a
Class I, Level of Evidence B –randomised studies.
b
Class I, Level of Evidence B –non-randomised studies.
c
Class I, Level of Evidence C –expert opinion.
d
Class IIa, Level of Evidence B –non-randomised studies.
e
Class IIa, Level of Evidence C –limited data.
f
Class IIa, Level of Evidence C –expert opinion.
g
Class IIb, Level of Evidence B –non-randomised studies.
h
Class IIb, Level of Evidence C –expert opinion.
i
Class III, Level of Evidence B –non-randomised studies.
j
Class III, Level of Evidence C –limited data.
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deliver adequate coronary, cerebral and systemic organ observational studies of OHCA, presumably due to
perfusion that is balanced against increasing the met- cerebral vasoconstriction. Where possible, patients
abolic demands of an already stressed heart through should be ventilated to normocarbia with a PaCO2
the use of fluids and vasoactive agents. A recent meta- of 35–45 mmHg. This may need to be individualised
analysis associated higher MAP with improved neuro- in the patient with coexistent pathology where more
logical outcome but it is not clear that improving MAP definitive evidence exists for an alternative ventilation
was responsible for the improved outcomes. strategy –for example, permissive hypercarbia in the
MCS theoretically offers improved systemic and setting of acute respiratory distress syndrome (ARDS).
coronary perfusion without necessarily increasing
myocardial oxygen consumption. The role of the intra-
aortic counterpulsation balloon pump (IABP) remains Targeted Temperature
controversial; and newer devices including ECMO and Management (TTM)
left ventricular assist devices (LVADs) are being used Post-cardiac arrest brain injury (as outlined above)
in selected patients in some specialist centres. is the major cause of morbidity and mortality in
Routine antiarrhythmic prophylaxis is not recom- comatose patients who are initially resuscitated from
mended in the absence of persistent dysrhythmia. OHCA. Multiple trials have demonstrated improved
neurological outcomes with targeted temperature
Oxygenation and Ventilation management to 32–36 °C in an attempt to mitigate the
Oxygen therapy after OHCA is controversial. There cascading cellular effects thought to be responsible
are conflicting retrospective data regarding whether for propagating neuronal cell death following ischae-
hyperoxia is associated with an increased mortality in mia and reperfusion (see Table 25B.2). Benefits were
post-cardiac arrest patients. A prospective, multicentre, most pronounced in patients with an initial shockable
randomised controlled trial of air versus supplemental rhythm (ventricular fibrillation (VF) or pulseless ven-
oxygen in STEMI patients who were not hypoxaemic tricular tachycardia (VT)).
demonstrated an increase in myocardial infarction size The practicalities of active TTM involve sig-
assessed at 6 months. In this context, it would seem pru- nificant resource allocation –equipment, education
dent to titrate inspired oxygen levels to achieve satura- and training –and are not without complexity and
tions of 94–98%. Both hypoxaemia and hyperoxia should complications. Continuous temperature monitoring
be avoided, but adequate peripheral perfusion and accu- is required. Cooling strategies need to address the
rate saturation monitoring are imperative before consid- induction and maintenance of TTM, and rewarm-
ering reducing inspired oxygen concentrations. ing. Options include infusion of ice cold fluid, sim-
In the comatose OHCA patient with ROSC an ple surface cooling with ice packs, or more formal
endotracheal tube (ETT) should be inserted if this systems with fluid or air circulating blankets, vests
was not done as part of the ALS resuscitation. Tube and limb wraps that include integrated control from
position should be confirmed with clinical examina- continuous temperature monitoring. More aggressive
tion, continuous (waveform) end-tidal carbon dioxide and invasive cooling strategies can include intravas-
monitoring and imaging (CXR or on CT chest scan if cular heat exchange catheters, body cavity lavage or
this is performed). the institution of MCS. The risk and benefit of each
Hyperventilation with subsequent hypocarbia has strategy need to be considered on an institutional and
been associated with worse neurological outcome in individual patient level.
Table 25B.2 Targeted temperature management

Comatose adult patients with ROSC after cardiac arrest should have TTM for VF/pulseless VT OHCAa; for non-VF/pulseless VT (i.e. ‘non-
shockable’)c and in-hospitala cardiac arrest.
Select and maintain a constant temperature between 32 °C and 36 °C during TTM.a
It is reasonable that TTM be maintained for at least 24 hours after achieving target temperature.f
Whether certain subpopulations of cardiac arrest patients may benefit from lower (32–34 °C) or higher (36 °C) temperatures remains
unknown, and further research may help elucidate this.
For footnotes see Table 25B.1.
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The potential physiological responses to cooling cardiorespiratory supports (WCRS) following prog-
need to be anticipated and addressed when they occur. nostication of a poor neurological outcome. Where
Shivering occurs as an autonomic response OHCA patients can be identified as having no pros-
to hypothermia and can limit the effectiveness of pect of meaningful neurological recovery, inappropri-
TTM. Strategies to mitigate shivering include the ate treatments can be avoided. However, the gravity of
use of short-acting sedative agents, opioid agonists the WCRS decision is such that prognostic assessment
and alpha-agonists but adequate temperature man- must be accurate and appropriate.
agement often requires the use of short-acting non- The self-fulfilling nature of a prognosis of poor
depolarising neuromuscular blocking agents. neurological outcome leading to WCRS and death
Bradycardia is common and can result in a means that biases are inherent in many of the earlier
reduced cardiac output. At lower temperatures sys- studies of prognostication. This may have been fur-
temic metabolic rate and oxygen consumption fall ther compounded by the use of sedative medications
and the bradycardia is thought to be associated with to facilitate TTM, from the effects of TTM on the
improvements in diastolic function. Systemic vascu- pharmacokinetic and pharmacodynamic properties
lar resistance may be increased where vasoconstric- of the medications, and potentially from the TTM
tion predominates, but may be reduced in the setting itself.
of a significant SIRS response to systemic ischaemia- Various clinical examination findings, investiga-
reperfusion. The net effect of the alterations to the tions and imaging methodologies have been exam-
adequacy of tissue oxygen delivery should be assessed ined for prognostic relevance in the pre-TTM and
on an individual basis. TTM eras (see Table 25B.3 and Figure 25B.3).
A cold diuresis from renal tubular dysfunction
may cause a relative hypovolaemia and significant
electrolyte disturbance. Mechanical Support
Insulin sensitivity is reduced at lower tempera- There is insufficient evidence to support routine use
tures and blood glucose should be measured regularly. of MCS –mechanical chest compression devices
Where insulin is used in hypothermia, it is important (MCCD) and/or ECPR –in OHCA.
to closely monitor blood glucose during rewarming as MCCDs have not been associated with improved
hypoglycaemia may occur. survival to hospital discharge nor with improved
Coagulation is impaired at lower temperatures neurological outcomes, and manual chest compres-
but this does not appear to be associated with a clini- sion remains the standard of care. The use of MCCDs
cally significant increase in bleeding rates. requires capital outlay for purchase and ongoing
Drug clearance is significantly reduced at lower costs associated with education, training and mainte-
temperatures and this must be taken into account nance. However, the appropriate use of MCCDs dur-
when prognostication is being considered. ing patient transfer can facilitate staff safety whilst
The perceived benefits of TTM have been demon- also minimising interruptions to chest compres-
strated in a time where a focus on bundles of post- sions. This includes transport in emergency vehicles
OHCA care has been instituted. It is unclear which between health care facilities, and within hospitals for
component of these treatment bundles has been intervention in the angiography suite. Critical care
responsible for the greatest improvements in out- practitioners should be familiar with the operation
come. Although TTM is thought to be integral to of these devices where they may be used in their cen-
these improved outcomes, the optimum temperature, tres. In accordance with current guidelines the focus
timing and duration of TTM remain to be elucidated. should remain on minimising interruptions to chest
compression.
Delayed Prognostication before ECPR is an area of growing interest and research.
Preliminary reports from specialist ECMO centres
Withdrawal of Cardiorespiratory with early institution of ECPR in selected patients
Supports have shown promising results when compared with
Post-cardiac arrest brain injury is the major cause conventional CPR –particularly in the setting of wit-
of mortality in OHCA patients but the mode of nessed, in-hospital cardiac arrest (IHCA) with a short
death in these patients is invariably withdrawal of interval from arrest to starting ECMO. Results for
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Table 25B.3 Timing of prognostication

The earliest time for prognostication using clinical examination in patients treated with TTM, where sedation or paralysis could be a
confounder, may be 72 hours after return to normothermia.h
The earliest time to prognosticate a poor neurological outcome using clinical examination in patients not treated with TTM is 72 hours
after cardiac arrest.b
This time until prognostication can be even longer than 72 hours after cardiac arrest if the residual effect of sedation or paralysis
confounds the clinical examination.e
Prognostication clinical examination

In comatose patients who are not treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is a
reasonable exam finding with which to predict poor neurological outcome (false positive rate (FPR), 0%; 95% CI, 0%–8%).d
In comatose patients who are treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is useful
to predict poor neurological outcome (FPR, 1%; 95% CI, 0%–3%).b
The findings of either absent motor movements or extensor posturing should not be used alone for predicting a poor neurological
outcome (FPR, 10%; 95% CI, 7%–15% to FPR, 15%; 95% CI, 5%–31%)i. The motor examination may be a reasonable means to identify the
population who need further prognostic testing to predict poor outcome.g
The presence of myoclonus (as distinct from status myoclonus) should not be used to predict poor neurological outcomes because of
the high FPR (FPR, 5%; 95% CI, 3%–8% to FPR, 11%; 95% CI, 3%–26%).i
In combination with other diagnostic tests at 72 or more hours after cardiac arrest, the presence of status myoclonus during the first 72
to 120 hours after cardiac arrest is a reasonable finding to help predict poor neurological outcomes (FPR, 0%; 95% CI, 0%–4%).d
Prognostication investigations
In patients who are comatose after resuscitation from cardiac arrest regardless of treatment with TTM, it is reasonable to consider the
bilateral absence of the N20 SSEP wave 24 to 72 hours after cardiac arrest or after rewarming a predictor of poor outcome (FPR, 1%; 95%
CI, 0%–3%).d
The persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent burst suppression on EEG after
rewarming, may be reasonable to predict a poor outcome (FPR, 0%; 95% CI, 0%–3%).g
Intractable and persistent (more than 72 hours) status epilepticus in the absence of EEG reactivity to external stimuli may be reasonable
to predict a poor outcome.g
In comatose post-cardiac arrest patients who are not treated with TTM, it may be reasonable to consider the presence of burst
suppression on EEG at 72 hours or more after cardiac arrest, in combination with other predictors, to predict a poor neurological
outcome (FPR, 0%; 95% CI, 0%–11%).g
Given the possibility of high FPRs, blood levels of NSE and S-100B should not be used alone to predict a poor neurological outcome.j
Prognostication imaging
In patients who are comatose after resuscitation from cardiac arrest and not treated with TTM, it may be reasonable to use the presence
of a marked reduction of the GWR on brain CT obtained within 2 hours after cardiac arrest to predict poor outcome.g
It may be reasonable to consider extensive restriction of diffusion on brain MRI at 2 to 6 days after cardiac arrest in combination with
other established predictors to predict a poor neurological outcome.g
For footnotes see Table 25B.1.
OHCA have been less promising and this is thought

to be related to the prolonged time between onset of
Organ Donation
Mortality rates in OHCA patients remain high even
cardiac arrest and institution of ECMO. Solutions cur-
after survival to ICU admission. Where patients ful-
rently being explored include the more rapid transport
fil broader criteria for organ donation this should be
of patients with OHCA to ECMO centres and the role
discussed with their family members and organ donor
of pre-hospital ECPR. Further economic and ethical
coordinators in line with hospital and national guide-
evaluation is required to establish the role of ECPR in
lines. In the setting of severe post-cardiac arrest brain
OHCA and how these patients should subsequently
injury patients may progress to brain death. Where
be managed.
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Cardiac arrest
Myoclonus
CT
Status
Days Controlled temperature
1–2
Rewarming
EEG - NSE
SSEP
Exclude confounders, particularly residual sedation
Unconscious patient, M=1–2 at > 72 h after ROSC

Magnetic Resonance Imaging (MR)
YES
Poor outcome
One or both of the following:
very likely
No pupillary and corneal reflexes
(FPR <5%, narrow
Bilaterally absent N20 SSEP wave(1)
Days 95% Cls)
3–5 NO
Wait at least 24 h
Two or more of the following

Status myoclonus ≤ 48 h after ROSC YES
High NSE levels(2) Poor outcome
Unreactive burst-suppression or status epilepticus on EEG very likely
Diffuse anoxic injury on brain CT/MRI(2)
NO
(1) At ≥24 h after ROSC in patients not treated

Indeterminate outcome with targeted temperature
Observe and re-evaluate (2) See text for details
Use multimodal prognostication whenever possible
Figure 25B.3 Prognostication algorithm. EEG electroencephalography; NSE neuron-specific enolase; SSEP somatosensory evoked
potentials; ROSC return of spontaneous circulation; FPR false positive rate; CI confidence interval.
cardiorespiratory supports are to be withdrawn, dona-

tion after circulatory death should be discussed.
Learning Points
• Post-resuscitation care is one of the four essential
links in the ‘chain of survival’ designed to
Family Screening improve survival in OHCA.
Coronary ischaemia remains the leading cause of • Post-cardiac arrest syndrome comprises:
OHCA. Where OHCA occurs in younger patients or
○ Post-cardiac arrest brain injury;
where investigations reveal no evidence of ischaemia,
○ Post-cardiac arrest myocardial
alternative diagnoses must be considered –including
dysfunction;
accelerated atherosclerotic disease, structural heart
disease, and primary arrhythmias. Structural heart ○ Systemic ischaemia-reperfusion response;
disease should be identified with imaging studies, and ○ Persistent precipitating pathology.
electrophysiological studies can help identify primary • The hospital interventions that have been
arrhythmias. In the event of death, a post mortem consistently associated with improved outcomes
examination should be conducted. Where a heritable after OHCA are:
condition is identified as the cause of OHCA, screen- ○ Early percutaneous coronary intervention
ing should be offered to family members –including (PCI);
clinical examination, electrophysiological studies, ○ Targeted temperature management;
cardiac imaging and potential genetic testing and ○ Delayed prognostication before withdrawal of
counselling. cardiorespiratory supports.
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• Prognostication should involve multiple International Liaison Committee on Resuscitation

assessment strategies, including examination, (American Heart Association, Australian and
neurophysiological testing and neuroimaging. New Zealand Council on Resuscitation, European
Resuscitation Council, Heart and Stroke Foundation
• Mechanical support in cardiac arrest is an of Canada, InterAmerican Heart Foundation,
evolving area. Further clinical, economic and Resuscitation Council of Asia, and the Resuscitation
ethical evaluation is required to establish the role Council of Southern Africa); the American Heart
of ECPR in both IHCA and OHCA. Association Emergency Cardiovascular Care
Committee; the Council on Cardiovascular Surgery
Further Reading and Anesthesia; the Council on Cardiopulmonary,
Perioperative, and Critical Care; the Council
Brrooks SC, Anderson ML, Bruder E, et al. Part 6: on Clinical Cardiology; and the Stroke Council.
Alternative Techniques and Ancillary Devices for Lippincott Williams & Wilkins, 2008, pp. 2452–2483.
Cardiopulmonary Resuscitation: 2015 American Heart Nielsen N, Wetterslev J, Cronberg T, et al. Targeted
Association Guidelines Update for Cardiopulmonary temperature management at 33°C versus 36°C after
Resuscitation and Emergency Cardiovascular Care. cardiac arrest. New England Journal of Medicine. 2013;
Circulation. 2015; 132(18 Suppl 2): S436–443. 369: 2197–2206.
Callaway CW, Donnino MW, Fink EL, et al. Part 8: Nolan JP, Soar J, Cariou A, et al. European Resuscitation
Post-Cardiac Arrest Care: 2015 American Heart Council and European Society of Intensive Care
Association Guidelines Update for Cardiopulmonary Medicine Guidelines for Post-resuscitation Care
Resuscitation and Emergency Cardiovascular Care. 2015: Section 5 of the European Resuscitation Council
Circulation. 2015; 132(18 Suppl 2): S465–482. Guidelines for Resuscitation 2015. Resuscitation.
Dragancea I, Rundgren M, Englund E, Friberg H, Cronberg European Resuscitation Council, American Heart
T. The influence of induced hypothermia and delayed Association, and International Liaison Committee on
prognostication on the mode of death after cardiac Resuscitation. Elsevier, 2015, 95: pp. 202–222.
arrest. Resuscitation. European Resuscitation Council, Soar J, Nolan JP, Böttiger BW, et al. European Resuscitation
American Heart Association, Inc., and International Council Guidelines for Resuscitation 2015: Section
Liaison Committee on Resuscitation. Elsevier, 2013, 3. Adult advanced life support. Resuscitation.
84: pp. 337–342. European Resuscitation Council, American Heart
Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Association, Inc., and International Liaison Committee
Advanced Cardiovascular Life Support: 2015 on Resuscitation. Elsevier, 2015, 95: pp. 100–147.
American Heart Association Guidelines Update for Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac
Cardiopulmonary Resuscitation and Emergency arrest syndrome: a review of therapeutic strategies.
Cardiovascular Care. Lippincott Williams & Wilkins, Circulation. 2011; 123: 1428–1435.
2015, pp. S444–S464.
Stub D, Smith K, Bernard S, et al. Air versus oxygen in ST-
Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest segment-elevation myocardial infarction. Circulation.
syndrome: epidemiology, pathophysiology, treatment, 2015; 131: 2143–2150.
and prognostication. A consensus statement from the
MCQs
1. The chain of survival does NOT include: (b) Hyperoxia post-ROSC is associated with improved
(a) Early CPR neurological outcomes
(b) Early defibrillation (c) Hypercarbia should never be allowed to occur in

these patients
(c) E-CPR
(d) Invasive arterial monitoring is indicated in the
(d) Post-resuscitation care post-resuscitation care phase
2. Regarding OHCA patients: 3. Current ALS guidelines suggest:
(a) Primary myocardial disease is an uncommon cause (a) Defibrillation should be delayed until the airway is
of arrest in this population secured
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(b) Interruptions to chest compression should be (d) Early percutaneous coronary intervention (PCI)
minimised should only be considered in patients with ST
(c) E-CPR has shown particularly promising results in elevation on their ECG
the OHCA population 5. Regarding neurological prognostication in OHCA
(d) The use of MCCDs (compared to manual chest patients:
compressions) is associated with improved neuro-
(a) A Glasgow coma motor score of 1 or 2 is a good
logical outcomes
predictor of poor neurological outcome
4. Regarding the ICU management of OHCA patients:
(b) Clinical neurological examination should be per-
(a) Observational studies suggest that the revers-
formed at least 36 hours after ROSC
ible ‘myocardial stunning’ effect can last for up to
6 hours (c) Multiple assessment strategies should be used,
(b) Routine arrhythmia prophylaxis with amiodarone including examination, neurophysiological testing
is recommended in all patients and neuroimaging
(c) Echocardiography may help to guide patient (d) Serum biomarkers can be used in isolation during
management prognostication
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Airway Emergencies
Chapter
26 Tom P Sullivan and Guillermo Martinez
Introduction The Obstructed Airway

The majority of patients admitted to an intensive care Airway obstruction is a blockage of the airway result-
unit require mechanical ventilation and consequently ing in reduced or impeded gas flow. The exact inci-
they are vulnerable to a number of airway complica- dence of airway obstruction in the cardiothoracic
tions. In these circumstances, airway emergencies ICU is unknown and it remains one of the most
such as airway obstruction, failed airway instrumen- challenging clinical scenarios for anaesthetists and
tation, airway device failure or postextubation prob- intensivists.
lems are life threatening situations. There are many causes of airway obstruction (see
In general, the management of the airway in the Table 26.1). Anatomically, the obstruction may be
intensive care unit is inherently more complex than supraglottic, glottic or subglottic. The clinical presen-
in the operating theatre, and complications of airway tation depends on both the location of the obstruct-
management are disproportionately higher. There are ing lesion and the time course of its development.
multiple patient, staffing and environmental factors Inspiratory stridor suggests a significant upper airway
that contribute to the higher complication rate. These obstruction with a reduction in airway diameter of at
factors may include the following: (i) patients are least 50%, whilst an expiratory wheeze indicates lower
physiologically compromised and frequently unsta- airway pathology.
ble; (ii) airway management is usually time critical;
(iii) it often occurs out-of-hours; and (iv) it is initially
managed by junior medical staff. Clinical Presentation and Assessment
The recognition of a compromised airway is the A focused history and examination allows rapid
crucial first step in managing an airway emergency. assessment of the patient. Important indicators of
Clinical features of significant airway compromise imminent airway compromise include hypoxia, agi-
often involve increased work of breathing, inspira- tation, inability to lie flat, failure to manage airway
tory stridor, obstructed breathing pattern, desatura- secretions and nocturnal symptoms. Importantly, any
tion and agitation. Untreated, the rapid development distress experienced by the patient may exacerbate the
of hypoxia, hypercapnia, acidosis and cardiovascular severity of the airway obstruction.
collapse may ensue. After initial assessment, the suspected site of the
Rapid assessment of the situation and prompt airway obstruction, the severity of the airway obstruc-
management is critical to achieve a successful out- tion and the overall condition of the patient will guide
come. Airway emergencies are dynamic and often further investigations. Initial tests may include a full
complex situations. The initial treatment priorities are blood count, inflammatory markers, blood cultures
to seek help and establish adequate oxygenation, while and a chest X-ray. In cases of suspected upper airway
preparation for deterioration or airway difficulty is obstruction, computed tomography is ideal to deline-
being arranged. In this chapter we will overview the ate the lesion. However, in patients unable to lie flat,
challenges associated with the instrumentation of the nasendoscopy exploration is the procedure of choice.
airway in critically ill patients, the prevention and man- In those with suspected lower airway obstruction due
agement of their airway complications, and the organi- to a mass lesion, computed tomography of the chest
sational aspects of airway safety in intensive care. and neck is indicated.
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Table 26.1 Causes of airway obstruction management decisions should be formulated after

Supraglottic Infection Ludwigs angina consultation between a senior anaesthetist and sur-
Epiglottitis geon. The procedure is ideally performed in theatre
Retropharyngeal abscess and it is critical that the airway plan is well prepared
Laryngotracheobronchitis and communicated, with all team members ready and
Inflammatory Angioedema the appropriate equipment in the room.
Anaphylaxis However, there is no universal management plan
Neurological Bulbar palsy for securing the obstructed airway. Patients with upper
Obstructive sleep airway obstruction should be assessed as to whether
apnoea intubation is possible or a tracheostomy under local
Foreign body anaesthetic is required.
Tumour In patients who are considered possible to intubate,
the airway plan may include awake fibreoptic intuba-
tion or gas induction. Caution should be exercised
Glottic Tumour Vocal cord polyp
Vocal cord tumour
when using awake fibreoptic intubation –the proce-
dure is often difficult and complete airway obstruction
Vocal cord palsy
may be caused by the fibreoptic scope or loss of airway
Laryngospasm
tone due to sedation or local anaesthesia. Regardless,
an experienced surgeon, tracheostomy tray and rigid
Subglottic Tracheal stenosis bronchoscope should be immediately available in the
Tracheomalacia event of failure to intubate.
External Goitre In patients with subglottic airway obstruction, the
compression Mediastinal mass exact site of obstruction should be identified prior
Foreign body to embarking on intubation, unless the patient suf-
fers an acute deterioration. The most important con-
siderations are whether a tracheal tube can be safely
Initial Management of the passed beyond the obstruction and identification
Obstructed Airway of an appropriate rescue plan. An awake fibreoptic
intubation may be an appropriate plan A, allowing
Acute or severe airway obstruction is a critical emer-
placement of the endotracheal tube beyond the site
gency. Initial supportive measures must include sup-
of obstruction. More distal tracheal obstruction pre-
plemental oxygen, sitting the patient upright and
cludes the use of tracheostomy as a rescue technique
establishing intravenous access and appropriate moni-
and requires the use of rigid bronchoscopy. In signifi-
toring. Deteriorating patients and those in extremis
cant tracheobronchial obstruction, venovenous extra-
will need their airway secured. The definitive treat-
corporeal membrane oxygenation may be considered
ment should focus directly on the cause of the airway
prior to securing the airway.
obstruction and is tailored to the individual patient.
Antibiotics, corticosteroids and nebulised adrenaline
may be effective for the treatment of upper airway
swelling and infections, including epiglottitis or croup.
The Failed Airway
Failed airway management is a leading cause of mor-
Anaphylaxis should be managed with intravenous or
bidity and mortality in intensive care. The Fourth
intramuscular adrenaline in accordance with local and
National Audit Project (NAP4) identified ten events
national guidelines. Foreign bodies may be dislodged
in 2009 of failed endotracheal intubation in the inten-
by coughing or postural changes. Some patients can
sive care unit and five of these deteriorated into a ‘can’t
require urgent surgical assistance that may include ear,
intubate, can’t oxygenate’ (CICO) situation, requiring
nose and throat, thoracic or cardiac surgery.
cricothyroidotomy or emergency tracheostomy.
The incidence of a ‘can’t intubate, can’t oxygen-
Advanced Airway Management ate’ scenario was estimated to be less than 1/10,000
Airway management in patients with severe in 1991, and has probably fallen since then due to
obstruction is a complex and high-risk process. All the advent of laryngeal masks. A thorough airway
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Chapter 26: Airway Emergencies
assessment will identify most patients with difficult tracheal access. Cannula cricothyroidotomy involves
airway, however, the positive predictive value of these the insertion of a large-bore cannula through the cri-
tests is poor. cothyroid membrane and use of a high pressure oxy-
Factors identified in NAP4 as associated with gen delivery device. This technique can provide rapid
failed intubation include patient obesity, known or rescue oxygenation; however it is not appropriate for
predictable difficult airways, trainees with limited ventilation and clearance of CO2. Further, the tech-
advanced airway experience, poor judgement and lack nique has reported high rates of failure, and inability
of equipment. to obtain a cannula cricothyroidotomy within five
Prevention of a ‘can’t intubate, can’t oxygenate’ attempts requires an alternative technique. The risks
scenario requires proper airway assessment and plan- of the technique include cannula displacement with
ning. Every intubation should have a plan A, B, C and potential to create significant surgical emphysema,
D as per the Difficult Airway Society (DAS) guidelines, barotrauma and volutrauma. A cannula cricothyroi-
with appropriate equipment ready, the patient posi- dotomy is an emergency and temporary oxygenation
tion optimised and experienced personnel present. technique that allows stabilisation of the patient. A
definitive airway should be established as a matter of
priority by percutaneous or surgical tracheostomy.
‘Can’t Intubate, Oxygenate (CICO) Emergency surgical tracheostomy is less familiar
‘Can’t intubate, can’t oxygenate’ exists when there have to intensive care and anaesthetic specialists and risks
been failed attempts at intubation, failed attempts at inadvertent endobronchial intubation. It may be per-
oxygenation (facemask and supraglottic airway device) formed by those with suitable expertise and experi-
and low or falling oxygen saturations. Identification ence, particularly in failed FONA.
of a CICO situation is imperative to good outcomes. Percutaneous tracheostomy is a technique famil-
Repeated failed attempts at endotracheal intubation iar to intensive care specialists, and presents a viable
risk further airway trauma whilst delaying appropri- alternative to establishing an emergency surgical
ate management. The reluctance to perform a surgical airway. The technique utilises a cannula cricothyroi-
airway has been identified as a contributor to mortal- dotomy initially. A wire is then inserted into the tra-
ity in CICO situations. chea, followed by a dilator and then a tracheostomy
The Difficult Airway Society published guidelines tube. Various tracheostomy sets exist, including single
for management of unanticipated difficult intubation, dilation sets. Current guidelines recommend scalpel-
including CICO. Failure to intubate necessitates that bougie as the initial technique as it is fast, has few
oxygenation, rather than intubation or ventilation, steps and it establishes a definitive airway. The alterna-
becomes the priority. Rapid development of severe tive techniques may be considered when the scalpel-
hypoxaemia, hypoxic brain injury and cardiovascular bougie approach has failed and suitable expertise is
collapse ensues if oxygenation is not re-established. available.
Help should be sought as soon as intubation is recog-
nised as difficult or failed. Oxygen Delivery Techniques
A variety of oxygen delivery techniques are available,
Rescue Techniques for CICO but a detailed discussion is included in Chapter 17. An
Oxygenation must be obtained emergently via front established surgical airway utilising a cuffed endotra-
of neck access (FONA), usually through the crico- cheal tube allows direct connection to most ventila-
thyroid membrane. The DAS guidelines recommend tors or bag-valve-mask devices via a 15 mm connector;
the scalpel-bougie technique as first-line approach for however, the use of a cannula presents a number of
FONA. This technique uses a cricothyroid incision limitations. In a CICO scenario, the upper airway is
with a scalpel, insertion of a bougie and rail-roading obstructed, and the main route of exhalation is via
of a small cuffed endotracheal tube. This technique the cricothyroidotomy cannula. Many oxygen deliv-
has higher success rates than a cannula technique and ery techniques, including jet ventilation devices, fail
may be more acceptable to anaesthetic and intensive to allow exhalation and continue to deliver oxygen to
care specialists. the patient, risking significant and rapid volutrauma.
Cannula cricothyroidotomy and surgical tra- Specially designed devices have an adequate exhala-
cheostomy are alternative techniques for emergency tion valve. In the absence of these devices, the oxygen
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Figure 26.1 https://www.das.uk.com/guidelines/icu_guidelines2017. Reproduced from Guidelines for the management of tracheal

intubation in critically ill adults, Higgs et al. (2017).
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Table 26.2 Complications of tracheostomy

Immediate Procedural complications Hypoxia
Hypercapnia
Acidosis
Loss of airway
Haemorrhage
Pneumothorax
Surgical emphysema
Oesophageal injury
Cricoid cartilage damage
Tracheostomy obstruction Cuff herniation
Occlusion by tracheal wall
Misplacement of tracheostomy Endobronchial intubation
False passage
Tracheal tube complications Puncture of tracheal tube cuff
Dislodgement of tracheal tube
Early Mechanical Dislodgement

Obstruction Secretions
Blood
Cuff herniation
Infection Tracheostomy stoma site
Tracheobronchial tree
Delayed Mechanical Dislodgement

Obstruction Secretions
Blood
Cuff herniation
Infection Tracheostomy site
Tracheobronchial tree
Ventilation associated pneumonia
Fistula to surrounding structure Tracheo-innominate artery fistula
Tracheo-oesophageal fistula
Persistent trachea-cutaneous fistula
Tracheal injury Tracheal and laryngeal stenosis
Tracheomalacia
delivery device should be disconnected whenever the upper airway obstruction and management of res-
patient is not actively ventilated through the cannula piratory tract secretions. It may also be performed
cricothyroidotomy. Regular training and familiarisa- for rescue airway management or electively in thea-
tion with local cricothyroidotomy equipment is essen- tre for major airway surgery or laryngectomy. The
tial to maintain high standards for the rescue of CICO EPIC study estimated approximately 16% of patients
patients. in UK intensive care units have a tracheostomy at any
one time.
Tracheostomies accounted for 50% (18/ 36)
Tracheostomy Emergencies airway events in the intensive care unit in NAP4.
Tracheostomy is commonly performed in the inten- Fourteen patients had their tracheostomy dis-
sive care unit for prolonged mechanical ventilation, lodged, resulting in seven deaths and four hypoxic
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Emergency tracheostomy management – Patent upper airway
Call for airway expert help

A Mapleson C system (e.g. ‘Waters circuit’) may help assessment if available
Use waveform capnography when available: exhaled carbon dioxide indicates a patent or partially patent airway
No Is the patient breathing? Yes
Call Resuscitation Team Apply high flow oxygen to BOTH

CPR if no pulse/signs of life the face and the tracheostomy
Assess tracheostomy patency
Remove speaking valve or cap (if present)

Remove inner tube
Some inner tubes need re-inserting to connect to breathing circuits
The tracheostomy tube is patent

Can you pass a suction catheter? Yes Perform tracheal suction
Consider partial obstruction
No Ventilate (via tracheostomy) if
not breathing
Deflate the cuff (if present) Continue ABCDE assessment
Tracheostomy tube partially

Yes obstructed or displaced
Is the patient stable or improving? Continue ABCDE assessment
No
REMOVE THE TRACHEOSTOMY TUBE
Look, listen & feel at the mouth and tracheostomy. Ensure oxygen re-applied to face and stoma
Call Resuscitation team No Yes Continue ABCDE

Is the patient breathing?
CPR if no pulse/signs of life assessment
Primary emergency oxygenation Secondary emergency oxygenation
Standard ORAL airway manoeuvres Attempt ORAL intubation

Cover the stoma (swabs/hand). Use: Prepare for difficult intubation
Bag-valve-mask Uncut tube, advanced beyond stoma
Oral or nasal airway adjuncts
Supraglottic airway device e.g. LMA
Attempt intubation of STOMA

Small tracheostomy tube/6.0 cuffed ETT
Tracheostomy STOMA ventilation
Consider Aintree catheter and fibreoptic
Paediatric face mask applied to stoma ‘scope/Bougie/Airway exchange catheter
LMA applied to stoma
National Tracheostomy Safety Project. Review date 1/4/14. Feedback & resources at www. tracheostomy.org.uk
Figure 26.2 Management of tracheostomy and laryngectomy airway emergencies. Reproduced from McGrath et al. (2012), with
permission from the Association of Anaesthetists of Great Britain & Ireland/Blackwell Publishing Ltd.
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brain injuries (see Table 26.2). In two-thirds of these Immediate assessment should be undertaken. The
cases, the dislodgement occurred on moving or inner tube or speaking device can be removed, leaving
turning. Two further patients had failure to place an the tracheostomy in situ. A suction catheter should be
elective tracheostomy in intensive care and two had inserted to assess the patency of the tracheostomy. If a
major haemorrhage post decannulation. Obesity suction tube cannot be passed, the tracheostomy cuff
was identified as a significant risk factor for trache- should be deflated to relieve the obstruction. If the
ostomy complications and capnography was used patient does not improve then the tracheostomy tube
infrequently. The high morbidity of tracheostomy should be removed.
complications led to the development of current
national guidelines. Airway Bleeding
Airway bleeding most commonly presents early post-
Dislodged Tracheostomy tracheostomy insertion, but may also present postde-
Tracheostomy dislodgement is the most commonly cannulation. Bleeding or infection complicates 5% of
lethal tracheostomy complication. Displacement percutaneous tracheostomies.
occurs with all types of securement devices; how- Tracheoinnominate artery fistula, caused by
ever patient turning and obesity were associated breaching of the tracheal wall into the innominate
with dislodgement. The infrequent use of capnog- artery, is a rare but frequently fatal cause of airway
raphy can lead to a delay in detection and worse haemorrhage, occurring days to weeks post tracheos-
outcomes. tomy insertion. It presents as massive airway haem-
A dislodged tracheostomy tube is an emergency orrhage, which requires immediate airway support.
and early recognition is crucial. Help and expert air- A tracheal tube may be advanced into the airway and
way assistance should be sought. Assessment must be the cuff inflated to tamponade the fistula before emer-
made immediately for airway, breathing and circula- gency surgery is performed.
tion (see Figure 26.2). Supplemental oxygen must be
applied to both the face and neck stoma.
In those patients who require airway instrumen-
Post Extubation Airway
tation, initial airway manoeuvres should be directed Emergencies
at the oral route, such as bag-mask ventilation and Extubation is an important but often neglected com-
supraglottic airways, whilst sealing the neck stoma. ponent of airway management. A stable airway is
Oxygenation may also be attempted via the stoma, removed and remains unsecured until the patient
using a small paediatric mask. Failure to oxygen- is able to maintain airway patency and protective
ate should lead to an attempt at oral intubation and reflexes. Most complications post extubation are
advancing the tracheal tube beyond the stoma, fol- minor. However, airway emergencies may occur due
lowed by attempted intubation via the stoma, careful either to airway obstruction or contamination.
not to intubate the bronchus. Ideally, this is under- The Difficult Airway Society published guidelines
taken using fibreoptic bronchoscopy guidance. The on extubation post anaesthesia, stratifying patients
use of capnography for the confirmation of a secured into ‘low-risk’ or ‘at-risk’ groups with corresponding
airway is mandatory. extubation algorithms.
Laryngectomy patients, however, have altered
anatomy with no upper airway connection to the tra- Unplanned Extubation
chea. All attempts at oxygenation and airway instru-
Inadvertent extubation is not uncommon, occurring
mentation in these patients should be directed to the
at a rate of one per 100 ventilator days. However, only
tracheostomy site.
four cases were reported in the NAP4 audit. Three of
these patients were obese, the fourth was a known
Blocked Tracheostomy Tube difficult airway and two patients suffered aspiration
Tracheostomy tubes may become blocked at any as a result. Capnography was not utilised in any of
stage due to blood, secretions, displacement or cuff these cases.
herniation. Clinical presentation includes dyspnoea, Accidental extubation typically occurred dur-
increased work of breathing and desaturation. ing patient movement, sedation breaks and minor
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airway manipulation. Risk factors for unplanned

extubation include higher levels of arousal, agitation
Airway Contamination
The airway may become contaminated with secretions,
and less experienced nursing staff. Identification
blood or foreign bodies. Airway contamination will
of inadvertent extubation is crucial to limit the
present with coughing, gagging or airway obstruction.
risk of complications such as aspiration, hypoten-
Initial management is supportive. The airway may
sion, arrhythmias, airway injury and respiratory
need to be secured by intubation and plans for a dif-
compromise.
ficult intubation need to be established. Care should
Not all patients will require reintubation.
be taken to suction out the airway prior to extubation.
Supplemental oxygen and supportive manoeuvres
may be adequate. Reintubation is more likely to be
required in patients with deeper levels of sedation, Systemic and Organisational
high oxygen requirements, high levels of pressure sup-
port or positive end-expiratory pressure and cardio-
Considerations
Airway emergencies in the intensive care unit are asso-
vascular instability.
ciated with high morbidity and mortality. Recognition
and diagnosis is often delayed, hindering effective
management. They may occur at any time and are
Airway Obstruction often managed by junior medical and nursing staff
Airway obstruction post extubation may occur sec- unfamiliar with airway equipment or management of
ondary to reduced airway tone, laryngospasm or complex airway emergencies. Numerous factors have
contamination of the airway. It is characterised by been identified that may reduce the rate of these com-
inspiratory stridor, respiratory efforts with reduced plications and improve outcomes.
airflow and desaturation. The treatment depends on
the cause.
Initial efforts should be focused on oxygena-
Staff and Training
tion. Jaw thrust and chin lift will frequently relieve Intensive care skill-
mix with variable experience in
obstruction due to drowsiness. An oropharyngeal airway emergencies should be minimised. All jun-
or nasopharyngeal airway may help and bag-mask ior medical staff should be familiar with basic airway
ventilation may be required. If the patient does management techniques and staff with experience in
not improve quickly, a secure airway should be advanced airway support should be available at all hours.
re-established. Staff education should focus on identifying those
Laryngospasm causes either partial or complete with difficult airways, their assessment and manage-
airway obstruction. It often occurs in response to stim- ment. Identification of potentially difficult airways
ulation when patients are emerging from anaesthesia. allows a defined plan to be made in the event of an
Airway blood or mucus causing irritation of the vocal emergency, including seeking assistance early. Airway
cords can result in laryngospasm. Initial management management education includes training in basic and
is supportive, with bag-mask ventilation utilising pos- advanced airway skills as well as management algo-
itive end-expiratory pressure. A strong jaw lift, known rithms for difficult and failed airways. Maintenance
as Larson’s manoeuvre, may break the spasm. If it con- of emergency airway skills, including ‘can’t intubate,
tinues, resedation and muscle relaxation will cause can’t oxygenate’ scenarios, may be best achieved with
the laryngospasm to cease. The increased respiratory simulation and skills sessions training.
effort with the closed glottis may cause negative pres-
sure pulmonary oedema. Equipment
Less common causes of airway obstruction post- All intensive care units should have access to a dif-
operatively include recurrent laryngeal nerve injury ficult airway trolley and fibreoptic bronchoscopy. As
and foreign body. Bilateral, rather than unilateral, specialists, it is important that intensivists are familiar
recurrent laryngeal nerve injury will cause upper air- with the contents and use of airway equipment avail-
way obstruction. Foreign bodies include swabs, teeth able in their unit. Additionally, medical staff should
and dentures. Risk factors include surgery on the be familiar and confident using a variety of different
upper airway and traumatic intubation. equipment.
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Capnography is a crucial monitor for intubated

and ventilated patients. Its use is universal in anaesthe-
Further Reading
Cook TM, Woodall N, Harper J, Benger J. On behalf
sia but variable in the intensive care unit. Capnography of the Fourth National Audit Project. Major
should be utilised for every intubation to confirm complications of airway management in the
endotracheal tube position as well as throughout the UK: results of the Fourth National Audit Project of
period the patient is intubated and dependent on a the Royal College of Anaesthetists and the Difficult
ventilator. Airway Society. Part 2: intensive care and emergency
departments. British Journal of Anaesthesia. 2011;
106: 632–642.
Planning and Preparation Da Silva PSL, Fonseca MCM. Unplanned endotracheal
extubations in the intensive care unit. Anesthesia &
The early identification of patients at risk for airway Analgesia. 2012; 114: 1003–1014.
complications and the recognition of an airway emer-
Flavell EM, Stacey MR, Hall JE. The clinical management
gency is important for best outcomes. Identification of of airway obstruction. Current Anaesthesia and Critical
patients with potential airway difficulty allows the for- Care. 2009; 20: 102–112.
mulation and communication of an appropriate plan
Greenland KB, Acott C, Segal R, Goulding G, Riley
should trouble strike. RH, Merry AF. Emergency surgical airway in life-
However, not all airway emergencies can be pre- threatening acute airway emergencies –why are we so
dicted and early recognition of an emergency remains reluctant to do it? Anaesthesia and Intensive Care. 2011;
crucial. A clearly formed management plan is critical; 39: 578–584.
however all plans can fail and the back-up plans (B, Heard AMB, Green RJ, Eakins P. The formulation and
C and D) are as important as the initial strategy. This introduction of a “can’t intubate, can’t ventilate”
must be communicated clearly with the team, expe- algorithm into clinical practice. Anaesthesia. 2009;
rienced staff must be available and equipment ready. 64: 601–608.
Henderson JJ, Popat MT, Latto IP, Pearce AC. Difficult
Airway Society guidelines for management of the
Summary unanticipated difficult intubation. Anaesthesia. 2004;
59: 675–694.
Airway emergencies in the intensive care unit are
complex situations associated with high rates of mor- Higgs BA, McGrath C, Goddard J. Rangasami G,
Suntharalingam R, Gale, TM. Cook and on behalf
bidity and mortality. Early identification of those at of Difficult Airway Society, Intensive Care Society,
risk allows thorough planning and management in a Faculty of Intensive Care Medicine, Royal College of
controlled and timely manner. The nature of airway Anaesthetists. British Journal of Anaesthesia. 2017; In
emergencies and complications necessitates that back- press. doi: 10.1016/j.bja.2017.10.021.
up plans with appropriately qualified staff and equip- Huggs A, McGrath BA, Goddard C, et al. and on behalf
ment are immediately available. of Difficult Airway Society, Intensive Care Society,
Faculty of Intensive Care Medicine, Royal College
of Anaesthetists. Guidelines for the management
Learning Points of tracheal intubation in critically ill adults. British
Journal of Anaesthesia. In press.
• Airway management in the intensive care unit is
Listello D, Sessler CN. Unplanned extubation.
associated with disproportionately high rates of
Clinical predictors for reintubation. Chest. 1994;
complications. 105: 1496–1503.
• Early recognition of emergencies allows
Mallick A, Bodenham AR. Tracheostomy in critically ill
preparation and planning. patients. European Journal of Anaesthesiology. 2010;
• The initial airway management should focus on 27: 676–682.
providing oxygenation. Mason RA, Fielder CP. The obstructed airway in head and
• Securing the airway can be a complex process. neck surgery. Anaesthesia. 1999; 54: 625–628.
Experienced personnel should be present and McGrath BA, Bates L, Atkinson D, Moore JA.
plans A, B, C and D ready in case of initial failure. Multidisciplinary guidelines for the management of
• All intubated and ventilator dependent patients tracheostomy and laryngectomy airway emergencies.
should have continuous capnography monitoring. Anaesthesia. 2012; 67: 1025–1041.
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Mort TC. Emergency tracheal intubation: complications Soar J, Pumphrey R, Cant A, et al. Emergency
associated with repeated laryngoscopic attempts. treatment of anaphylactic reactions –Guidelines
Anesthesia & Analgesia. 2004; 99: 607–613. for healthcare providers. Resuscitation. 2008;
Patel A, Pearce A. Progress in management of the 77: 157–169.
obstructed airway. Anaesthesia. 2011; 66: 93–100. Vincent JL, Suter P, Bihari D, Braining H. Organisation
Popat M, Mitchell V, Dravid R, et al. Difficult Airway of intensive care units in Europe: lessons from
Society Guidelines for the management of tracheal the EPIC study. Intensive Care Medicine. 1997;
extubation. Anaesthesia. 2012; 67: 318–340. 23: 1181–1184.
MCQs
1. Time to desaturation following the onset of apnoea is (d) Cannula cricothyroidotomy allows adequate
influenced by: exhalation
(a) The muscle relaxant used (e) If rescue cannula cricothyroidotomy is successful,
(b) The adequacy of preoxygenation the patient should be woken up
(c) The patient’s age 4. In the intensive care unit, which of the following is
true regarding emergency airway management?
(d) Lying the patient supine
(a) Oesophageal injury is a recognised and unavoid-
(e) Insufflation of air able complication of airway management
2. Regarding patients with tracheostomy, which of the (b) Suxamethonium is the preferred muscle relaxant,
following is true? due to its quick offset in case of a failed airway
(a) The use of capnography will prevent complications (c) Preoxygenation may be suboptimal
from tracheostomy displacement
(d) Capnography should be used if a difficult intuba-
(b) In suspected airway blockage, the tracheostomy tion is anticipated
should be removed immediately
(e) Airway rescue with a laryngeal mask is not appro-
(c) Oral endotracheal intubation is not possible in priate, as the patients are usually unfasted
patients with tracheostomy
5. In postoperative patients after extubation, which of
(d) Capnography should be utilised in ventilator the following is true?
dependent tracheostomy patients
(a) Signs of airway obstruction require immediate
(e) Laryngectomy patients may be oxygenated ade- attention and re-intubation
quately by facemask oxygenation
(b) Laryngospasm may respond to positive end-expira-
3. Regarding ‘can’t inubate, can’t oxygenate’ scenarios, tory pressure
which of the following is true?
(c) A hoarse voice does not indicate an airway injury
(a) An emergency call for help should be made after
failed intubation and inability to oxygenate with a (d) Vomiting is unlikely to lead to pulmonary
supraglottic airway device aspiration
(b) After three failed attempts at cannula cricothy- (e) If reintubation is required, it may be more difficult
roidotomy, emergency tracheostomy should be than previous attempts
attempted
(c) If a cannula cricothyroidotomy is successful and
a laryngeal mask is in place, the laryngeal mask
should be left in situ
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Chest Pain as a Symptom on the

Chapter
27 Cardiothoracic Intensive Care Unit

Will Davies
Introduction Given the above issues a focused approach to his-

tory taking is required. The mainstays of site, charac-
Chest pain as a symptom can lead to over 400 eventual
ter, radiation, onset, severity, exacerbating factors and
diagnoses. Up to one third of those patients admit-
timing all still apply although many of these will be
ted to an acute medical unit may have chest pain as a
very dependent on the preceding interventions and
component of their presenting complaint. Chest pain
current therapy that the patient is undergoing. The
is almost ubiquitous in patients admitted to the car-
new onset of a complaint of chest pain, therefore,
diothoracic intensive care unit (CICU). For example,
requires a flexible approach to clinical assessment
the preoperative patient with ischaemic heart disease
to rule out the most important and potentially life
may experience the full range of associated symp-
threatening causes in a systematic fashion.
toms from central crushing pain with radiation, to
the silent myocardial infarction of a long-term dia-
betic with associated neuropathy. Once these same Clinical Examination
patients have undergone surgical revascularisation, The role of clinical examination in the CICU can often
this ischaemic pain will probably be substituted for be overlooked. With all the intensive monitoring and
the dull, central tenderness of a median sternotomy, real time data that are now available, including bedside
or the pleuritic pain of a residual pneumothorax irri- transthoracic echocardiography and easy access com-
tated by the intercostal chest drains. The evaluation puterised tomography, the stethoscope can become
and subsequent treatment of chest pain on the CICU a vestigial appendage. However, this patient popula-
is vital to enhance the clinical outcome of this patient tion with positive pressure ventilation and invasive
population. procedures is particularly prone to complications
In this chapter we will endeavour to discuss the such as tension pneumothorax that need to be rapidly
rapid yet thorough assessment of chest pain as a assessed, diagnosed and treated to avoid unnecessary
symptom, the initial examination and investigation morbidity and potential mortality. Indeed, the CICU
strategy required, and outline the emergent therapeu- patient is at particular risk when transferred from the
tic options required for each differential diagnosis. controlled environment of the unit to other depart-
ments for investigation, and the role of clinical assess-
History ment must not be forgotten.
As with all clinical encounters the greatest aid to
formulation of an accurate differential diagnosis is a Differential Diagnosis
thorough clinical history. Several confounding factors The elective patient recovering on the CICU is likely
exist in the ICU patient that make the history less reli- to have been thoroughly investigated prior to admis-
able. The spectrum of confounders ranges from those sion. Many of the emergent admissions will also have a
patients that are sedated and ventilated, through the diagnosis underlying their chest pain by the time they
heavily narcotised and disorientated, to the patient arrive. However, these critically unwell and increas-
with ‘distraction’ pains who may under-report symp- ingly aged patients are prone to further, sometimes
tomatic changes. These challenges can result in unrelated, pathologies. Thus a physician must have
important delays in the detection of the pathology a widespread understanding of those conditions that
underlying chest pain. most commonly occur in the CICU patient.
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It is beyond the scope of this chapter to cover all of emergent cardiology consultation to rule out acute
the differential diagnoses the CICU staff may encoun- stent thrombosis requiring repeat intervention. The
ter in the patient with chest pain. However, we will second most common cause of postprocedural chest
aim to discuss those that are most common, those that pain in this group is a technical problem with the
are less common but life threatening, and those that stent placement, either an inflow or outflow coro-
are rare but need highlighting to ensure they are not nary artery dissection, or perhaps the obstruction of
overlooked. a side branch. Finally, the role of untreated bystander
disease is important as lesions that remain in other
Myocardial Ischaemia vessels may well become symptomatic in the high cat-
echolamine milieu that exists post PPCI.
Most of the patients that arrive on the CICU are likely
to have undergone some investigation into their coro-
nary vasculature, be it an invasive coronary angiog- Postsurgical Revascularisation
raphy or some form of non-invasive functional or
The rate of postoperative myocardial infarction fol-
anatomical test. In fact, the majority of such patients
lowing coronary artery bypass grafting is estimated to
will be admitted to the CICU to recover from a proce-
be between 5 and 10%. The incidence of graft related
dure, performed either percutaneously or surgically,
ischaemia is thought to be approximately 3%. In the
to improve the vascular supply of the myocardial bed.
intubated patient the clues to infarction and ischae-
These patients are not, however, immune from further
mia are persistent low cardiac output state, dysrhyth-
myocardial ischaemia.
mia, evolving ECG changes and new regional wall
motion abnormalities on echocardiographic imaging.
Postpercutaneous Coronary Intervention The routine use of biochemical markers of myocardial
Primary percutaneous coronary intervention is now damage is unlikely to be useful in the diagnosis in this
the revascularisation method of choice for patients population. In the awake patient, the chest pain of
presenting with an ST elevation myocardial infarc- myocardial ischaemia can be difficult to differentiate
tion. The admission rate to the CICU following this from the postoperative sternal wound pain although
procedure is around 5% and has been rising steadily any patient describing their usual angina should be
year on year. The majority of these patients are intu- investigated further. Patients in whom early graft fail-
bated and ventilated in the periarrest period in the ure is suspected have a significant adverse outcome
community, although some will require ventilation unless treated promptly.
during the PPCI procedure itself. If the cardiac arrest A second form of postprocedural cardiac ischae-
is prolonged then these patients will undergo a period mia is that induced by poor myocardial protection.
of cooling, or at least avoidance of hyperthermia, to This is difficult to diagnose and may present as a
aid neurological recovery. global reduction in left or right ventricular function
A particular challenge in the ventilated patient with associated haemodynamic compromise requir-
post PPCI is the administration and absorption of dual ing inotropic support.
antiplatelet medication. The risk of acute stent throm- Even in the patient with apparently unobstructed
bosis in this population is tenfold that of the spontane- coronary arteries who undergoes cardiac surgery, for
ously ventilating patient, with a mortality approaching example for a valve replacement, there is a risk of both
40%. It is, therefore, important to ensure that patients plaque rupture and importantly embolic obstruc-
receive and are absorbing the dual antiplatelets as pre- tion of the coronaries. This is particularly prevalent
scribed by the interventional cardiology team, and that in those patients with dilated atria and preoperative
premature cessation is avoided in all but life threat- atrial fibrillation. One final consideration is the occlu-
ening bleeding. In those patients who are unable to sion of the coronary ostia by the stent struts on a pros-
absorb enterically, alternatives include administration thetic aortic valve.
per rectum or substitution for an intravenous agent, A further mechanism of potential coronary flow
for example the glycoprotein IIb/IIIa inhibitors such as limitation is the phenomenon of coronary vasospasm.
abciximab, eptifibatide and tirofiban. This is often difficult to diagnose and is particularly
Any chest pain with concomitant ECG changes prevalent at the time of high catecholamine drive,
in the post PCI cohort of patients should trigger an such as during extubation. Intravenous vasodilators
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Chapter 27: Chest Pain as a Symptom
usually allow rapid resolution and prevent the lasting show the classic widened mediastinum, and contrast
damage of infarction. enhanced computed tomography has become the first
line in investigation. In those centres with expertise
Aortic Dissection in transoesophageal echocardiography, this imaging
Acute aortic dissection is the most common life modality has the advantage of being both sensitive
threatening pathology of the thoracic aorta and car- and specific, and also relatively rapidly performed.
ries a mortality of 1% per hour in the early stages. In Once diagnosed, type A aortic dissection is ini-
the simplest Stanford classification, type A aortic dis- tially treated by stabilisation of the patient using intra-
section involves the ascending aorta, whereas type B venous beta blockade. Thereafter, emergent surgery
dissections are those that do not involve the ascending to obliterate the false lumen and repair the ascending
aorta. This classification is useful, as type A dissec- aorta using an interposition graft is required.
tions benefit from emergent surgical repair, whereas Postprocedural management requires tight blood
type B aortic dissections are best managed medically pressure control with beta-blocker therapy providing
unless they become complicated. Type A aortic dis- the pharmacological mainstay. Various authors have
sections are more common in patients in their sixth reported survival rates of between 50 and 90% 1 year
and seventh decades, whereas type B dissections typi- following acute type A aortic dissection.
cally affect the elderly.
Although traditionally thought to be associated Superior Vena Cava Syndrome
with the connective tissue disorders such as Marfan, Although originally described as occurring in con-
Loeys– Dietz and Ehlers– Danlos syndromes, more junction with an infective cause, the most common
common predisposing factors include hypertension cause of superior vena cava syndrome (SVCS) world-
and bicuspid aortic valve anatomy. In the CICU setting, wide is now malignancy of the lung, breast or medi-
the physician must always be cognisant of the postsur- astinal nodes. Of particular concern to the patients
gical patient with sudden onset of intrascapular pain under consideration in this chapter, is the increasing
and haemodynamic instability. Any instrumentation incidence of iatrogenic SVCS secondary to device
of the ascending aorta, be that percutaneously with insertion, be those permanent pacemakers, implant-
ostial coronary stent placement, or surgically during able cardiac defibrillators or vascular access catheters.
aortic cannulation for cardiopulmonary bypass or Although most commonly diagnosed due to the pres-
during aortic valve replacement, may subsequently ence of distended neck and chest wall veins, cough,
cause separation of the layers of the aortic wall. Rarely, dyspnoea and facial swelling, several authors report
reports have been published of aortic dissection fol- the presence of a dull chest ache, mimicking that of
lowing cocaine use, during heavy lifting and during cardiac ischaemia. Treatment very much depends
systemic inflammatory vasculopathy. Although per- on the underlying aetiology, with external neoplas-
haps the most feared complication of pregnancy, dis- tic compression being best treated with debulking
section during pregnancy is relatively uncommon. therapies be those chemotherapeutic or surgical.
The typical chest pain associated with aortic dis- Thrombosis can be successfully reversed with throm-
section is said to be a searing or tearing pain that starts bolysis and anticoagulation, and some cases require
in the chest and rapidly radiates to the intrascapu- stenting to secure long-term patency.
lar region. Immediate complications include right
coronary artery occlusion and associated inferior
ST elevation, cardiac tamponade, acute aortic valve Vascular Air Embolism
insufficiency and neurological deficit. Atypical pres- The CICU has evolved over the last few decades
entations include renal failure of uncertain aetiology such that the average unit has a plethora of patients
due to loss of the renal arterial supply, and mesenteric undergoing various stages of organ support. Wide-
ischaemia manifest by rising serum lactate, abdomi- bore vascular access catheters can be connected to
nal pain and frequently loose stools. The loss of a continuous venovenous haemofiltration machines,
peripheral pulse was only present in 19% of patients extracorporeal membranous oxygenators, rapid
recorded in the International Registry of Acute Aortic infusers and ventricular assist devices. All of these
Dissection series. In 15% of patients with an acute life support technologies have the potential to
aortic dissection the chest radiograph will fail to allow the accidental entrainment of air into the
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circulation. Clinically, this often manifests as chest and bridging to recovery is seldom necessary. Even in
pain, dysrhythmia, right sided heart failure and cases of acute cardiac decompensation, the majority of
dyspnoea. A venous air embolus can sometimes patients make a full recovery and preserve their myo-
manifest as an arterial issue, such as stroke or myocardial function long term.
cardial infarction due to the passage from the right
atrium to the left atrium through a patent foramen Cardiac Tamponade and Myocardial
ovale or atrial septal defect.
The immediate management of vascular air Rupture
embolus is to identify the source and eliminate fur- Cardiac tamponade is defined as the compression of
ther entrainment. In the case of the patient in cardiac the cardiac chambers due to the accumulation of fluid,
arrest then vigorous cardiopulmonary massage has pus, blood clots or gas in the pericardial space. In the
been shown to be beneficial. As with all iatrogenic CICU environment the most common causes are the
complications, vigilant prevention is always better accumulation of blood post cardiac surgery, follow-
than the cure. ing percutaneous coronary intervention complicated
by coronary artery perforation or myocardial rupture.
The triad of high venous pressure, low systemic arterial
Pericarditis and Myocarditis pressure and muffled heart sounds is often observed.
Both myocarditis and pericarditis are usually caused The presence of pulsus paradoxus, defined as a fall
by an acute inflammatory process that may be second- in arterial pressure of greater than 10 mmHg during
ary to a viral infection, an autoimmune inflammation inspiration, can often be determined by observing the
or the presence of a toxin, either exogenous or from respiratory variation of the arterial line trace during
the accumulation of a metabolite. They may occur the ventilatory cycle. However, this clinical sign is
synchronously or can be seen as separate diagnoses. In not pathognomonic, and can also be seen in haemor-
Western countries most cases of myocarditis in previ- rhagic shock, massive pulmonary embolus and severe
ously healthy individuals are caused by enteroviruses, obstructive pulmonary disease.
especially Coxsackie B. Other less prevalent causes The most useful and immediate bedside test in the
include Lyme disease, caused by Borrelia burgdorferi, CICU environment is the echocardiogram, which typ-
Chagas’ disease, caused by Trypanosoma cruzi (com- ically confirms a pericardial collection, diastolic com-
mon in South America), and Kawasaki disease. promise of the right ventricle, the loss of respiratory
The prevalence is difficult to determine, as many variation in the IVC diameter, and greater than 25%
cases are mild and may be subclinical. Patients usually respiratory variation in the transmitral and transtri-
present with myalgia, malaise, cough or GI upset, and cuspid Doppler parameters. The treatment of cardiac
fever. The risk of fatal arrhythmia may persist for sev- tamponade is drainage of the pericardial collection,
eral weeks after the onset of symptoms, and appears to either percutaneously using CT or echo guided peri-
be linked to strenuous exercise. The chest pain of both cardiocentesis, or by re-exploration of the median
myocarditis and pericarditis may mimic that of acute sternotomy post cardiac surgery.
myocardial infarction, and in the early stages of the Myocardial rupture is an infrequent complication
illness the ECG may also be suggestive of an ST eleva- of myocardial infarction, occurring in approximately
tion MI. The typically scooped ST segment elevation 2% of patients who have had unsuccessful or delayed
and PR depression classically reported in pericardi- revascularisation, but carries a high mortality due to
tis may take several hours to develop. Both echocar- cardiac tamponade. Clinical features that aid the diag-
diography (which may show a regional wall motion nosis are a sudden onset of cardiovascular collapse,
abnormality in focal myocarditis) and troponin levels chest pain and jugular venous distension. Surgical
(which are frequently raised) are also poor differentia- repair is often fraught with the difficulty of very fri-
tors. Many of these patients who present to the cardi- able tissues.
ologist will, therefore, be investigated with an invasive
coronary angiogram. Tension Pneumothorax
Once recognised, the treatment of both myo- Pneumothorax is particularly common in the post-
carditis and pericarditis is largely supportive. operative patient on the CICU. However, the onset of
Complications of cardiac failure are relatively rare a tension pneumothorax may be insidious, and must
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Chapter 27: Chest Pain as a Symptom
be recognised and treated swiftly to avoid potentially distress, especially in postmenopausal female patients
fatal consequences. More details of its management with unobstructed coronary arteries. The Japanese
will be discussed in Chapter 28. term takotsubo means octopus pot, as the shape of the
left ventricle with the typical apical ballooning is said
Gastrointestinal Causes of Chest Pain to resemble the pot used by fishermen for catching
There are several well- recognised gastrointestinal octopodes. The syndrome often presents with severe
causes of chest pain that are often overlooked in the chest pain, anterior ST elevation and a raise in cardiac
initial assessment of the patient on the CICU. In biomarkers. It can, on occasion, cause cardiac arrest.
the postoperative period the presence of a ruptured The course is usually self- limiting with support-
oesophagus secondary to transoesophageal echo- ive care, but it can recur in up to one third of cases.
cardiography may be difficult to differentiate from a Various pathogenic mechanisms have been proposed
pneumothorax caused by the inadvertent opening of including vasospasm of the coronary vasculature
the pleural space. The leakage of gastric contents into secondary to a high catecholamine drive, although
the thorax can be insidious, and the subsequent sepsis a neurogenic mechanism of myocardial stunning, as
difficult to manage unless a high clinical suspicion is seen during acute neurological events, has also been
maintained. considered.
Cholecystitis is another mimic of acute myocardial
infarction, with right upper quadrant or epigastric Conclusion
pain, symptoms of sympathetic overdrive and even Chest pain as a symptom is almost ubiquitous
inferior ST elevation on the 12-lead ECG. A compli- amongst patients on the cardiothoracic ICU.
cation of a common bile duct stone, pancreatitis is Without a broad understanding of the myriad of
also seen in the critically unwell patient and serum or underlying diagnoses the ICU clinician may not be
urinary amylase assays can aid in the diagnosis. The able to rapidly identify those that are life threaten-
stress response to critical illness also raises the acidity ing versus those that are benign. The role of clinical
of the contents of the upper gastrointestinal tract and examination must not be forgotten in these days of
can lead to gastric ulceration and haemorrhage and sophisticated monitoring and the easy availability of
the subsequent chest pain. diagnostic imaging.
Wound Pain and Sternal Dehiscence Learning Points

Although sternal wound dehiscence is a rare compli- • A broad understanding of the differential
cation of cardiac surgery, it is associated with signifi- diagnoses underlying chest pain as a symptom
cant morbidity and mortality. Preoperative risk factors is vital to rapid assessment and diagnosis in
include diabetes mellitus, obesity, chronic obstructive the CICU.
pulmonary disease and smoking. Operative factors
• The mortality of an intubated and ventilated
include a long cardiopulmonary bypass time, post-
patient post primary PCI is tenfold that of a
operative haemorrhage, re-exploration of the wound,
spontaneously ventilating patient.
prolonged ventilation and the need for tracheostomy.
• The survival following type A aortic dissection
The conscious patient often complains of sternal pain,
is directly related to the time taken to
and CT scanning of the thorax can reveal the ster-
diagnosis and subsequent initiation of definitive
nal dehiscence, even in patients with little evidence
treatment.
of skin breakdown. Treatment varies from intrave-
• Several gastrointestinal causes of chest pain are
nous antibiotics through to complete sternotomy and
commonly seen in patients on the CICU and
reconstruction.
these diagnoses can be easily overlooked by the
unwary.
Takotsubo Cardiomyopathy
Takotsubo cardiomyopathy was first described in the
early 1990s and is a reversible left ventricular apical Further Reading
ballooning that may mimic acute myocardial infarc- Braverman AC. Acute aortic dissection. Circulation. 2010;
tion. It is typically precipitated by acute emotional 122: 184–188.
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Figueras J, Alcalde O, Barrabés JA, et al. Changes in Spodick DH. Acute cardiac tamponade. New England
hospital mortality rates in 425 patients with acute Journal of Medicine. 2003; 349: 684–690.
ST-elevation myocardial infarction and cardiac Virani SS, Khan AN, Mendoza CE, et al. Takotsubo
rupture over a 30-year period. Circulation. 2008; cardiomyopathy or broken heart syndrome. Texas
118: 2783–2789. Heart Institute Journal. 2007; 34: 76–79.
Oakley CM. Myocarditis, pericarditis and other pericardial
diseases. Heart. 2000; 84: 449–454.
MCQs
1. Following primary PCI, dual antiplatelet therapy (c) Is most commonly caused by intrathoracic
can be: malignancy
(a) Safely withheld for 48 hours post procedure (d) Does not cause chest pain
(b) Substituted for a glycoprotein IIb/IIIa inhibitor in (e) Should not be treated with thrombolysis
those patients who are not absorbing orally 4. In the absence of a pathological communication
(c) Discontinued with signs of non-life-threatening between the right and left heart, an air embolus should
bleeding not present with:
(d) A significant cause of a low platelet count (a) Dysrhythmia
(e) Omitted until the patient is spontaneously (b) Chest pain
ventilating (c) Stroke
2. Type A aortic dissection: (d) Right sided cardiac failure
(a) Typically results in a loss of a peripheral pulse (e) Dyspnoea
(b) Is reliably diagnosed on chest radiography 5. Takotsubo cardiomyopathy is uncommonly associ-
(c) Is more common in the elderly ated with:
(d) Can be effectively treated medically (a) Postmenopausal women
(e) May present with chest pain and diarrhoea (b) Cardiac arrest
3. Superior vena cava syndrome: (c) Severe coronary artery disease
(a) Is declining in incidence (d) Left ventricular apical ballooning
(b) Is unlikely to be iatrogenic (e) Long-term cardiac failure
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Chapter
Acute Dyspnoea and Respiratory Failure
28 Ken Kuljit Parhar
Introduction display dyspnoea without respiratory failure, and vice

versa, some patients can be hypoxic or hypercarbic
Respiration is a complex process during which gas
without the symptoms and signs of dyspnoea. The
exchange occurs between the respiratory system of
match of the two entities can give a clue to the dura-
the patient and the surrounding atmosphere. The two
tion of the problem, adaptive mechanisms and home-
major functions of the respiratory system are to oxy-
ostatic control of the patients.
genate the blood and to clear carbon dioxide (CO2)
through ventilation of the lungs. Appropriate respi-
ration requires several intact physiological pathways Hypoxaemic Respiratory Failure
including the central and peripheral nervous systems, There are several pathophysiological mechanisms
the respiratory muscles, the cardiopulmonary system, through which hypoxaemic ARF can occur, includ-
and an appropriate oxygen carrying capability with ing inadequate alveolar oxygen concentration (PAO2),
red blood cells. Pathological disruption of any of these ventilation-perfusion mismatch (V/Q), shunt, diffu-
systems can result in respiratory dysfunction. sion abnormalities and increased venous admixture
Dyspnoea (breathlessness) is a symptom and sign. (Figure 28.1). The most common cause of hypoxaemia
It is described by patients as difficulty with either in ICU patients is V/Q mismatch.
inspiration, expiration or both. As a sign dyspnoea
presents with involvement of accessory respiratory Inadequate Alveolar Oxygen (PAO2)
muscles and general distress. Dyspnoea is frequently Inadequate alveolar oxygen is most often caused by
but not exclusively associated with respiratory failure. either hypoventilation or a low partial pressure of
Dyspnoea can be caused by both physical and psycho- inspired oxygen.
logical stimuli. Hypoventilation results in hypoxaemia through
Dyspnoea as a sign is frequently obvious and most two mechanisms: a reduction in the PAO2–PaO2 gra-
often associated with tachypnoea. Use of accessory dient that causes a fall in PaO2 due to acidosis from
respiratory muscles is a common sign. Acute dyspnoea inadequately cleared CO2, resulting in a rightward
leads to fatigue due to increased work of breathing. shift of the oxyhaemoglobin dissociation curve and
Acute respiratory failure (ARF) is defined as the lower affinity of haemoglobin for O2.
inability to meet the metabolic requirements of the The second mechanism of low alveolar oxygen is
patient through a failure of either oxygenation or uncommon in the ICU population. It more commonly
ventilation. ARF can therefore be divided into two occurs at high altitudes where the partial pressure of
distinct subtypes including hypoxaemic respiratory the atmosphere is much lower than at sea level. It may
failure (type 1) resulting in low arterial oxygen (PaO2) also happen in an airplane where the cabin pressure is
or hypercarbic respiratory failure (type 2) resulting in not pressurised to sea level but to a higher elevation
elevated arterial CO2 (PaCO2). (6000–10,000 feet).
ARF is a common indication for admission to the The alveolar–arterial (A–a) gradient calculation is
intensive care unit (ICU), and can account for 17–56% a measure of the efficiency of alveolar gas exchange
of all admissions. and can be used to determine whether hypoventilation
The relationship between dyspnoea and acute res- is the cause of a low PaO2 (Figure 28.2). The normal
piratory failure is variable. Some patients suffer and A–a gradient is 10–20 mmHg; it is influenced by age
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Respiratory failure
Hypoxaemic Hypercarbic
Low Increased Increased Increased Decreased

V/Q Diffusion
alveolar Shunt venous CO2 dead alveolar
mismatch abnormality
oxygen admixture production space ventilation
Figure 28.1 Common aetiologies of respiratory failure within the ICU.
PaCO2
Alveolar – Arterial (A–a) oxygen gradient = PiO2 – – PaO2
R
Partial pressure of inspired oxygen (PiO2) = FiO2 (PB – water vapour pressure)
Thus:
PaCO2
Alveolar – Arterial (A–a) oxygen gradient = FiO2 (760 – water vapour pressure) – – PaCO2
R
Figure 28.2 Calculation of an alveolar–arterial (A–a) oxygen gradient. R respiratory quotient (VCO2/VO2) = 0.8, PaO2 arterial oxygen
concentration, FiO2 fraction of inspired oxygen, PaCO2 arterial CO2 concentration, PB (barometric pressure) = 760 mmHg at sea level, water
vapour pressure = 47 mmHg.
and increases with each decade of life. Hypoxaemia more than ventilated (low V/Q). In aggregate the lung
with a normal A–a gradient is suggestive of hypoven- has an overall matched V/Q ratio of approximately
tilation. The patient’s history can be used to rule out 1. Body position, posture and lung volumes, as well as
low inspired partial pressure of O2 in most cases, and age, can influence V/Q ratios in normal lungs.
the A–a gradient in this situation should be normal Any disease process that affects the lung paren-
as well. chyma can influence V/Q ratios (Figure 28.3). For
example low V/Q ratios are associated with processes
Ventilation and Perfusion Mismatch that impair ventilation such as bronchoconstriction,
Ventilation and perfusion (V/ Q) mismatch is the or secretions from pneumonia. High V/Q ratios are
most common mechanism for hypoxaemia within associated with processes that impair perfusion such
the ICU. In a normal upright lung there is a degree of as pulmonary embolism, or that lead to increased ven-
regional V/Q mismatch as the apices of the lung are tilation due to large tidal volumes such as emphysema.
ventilated more than perfused (high V/Q), in contrast The lung vasculature has mechanisms to attempt
to the bases of the lungs, which are perfused much to match V/Q and maintain an equal ratio such as
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Chapter 28: Acute Dyspnoea and Respiratory Failure
Airway Narrowing
Emphysema
Secretions
V V
V
Q Q Q
Pulmonary Embolism
Normal V/Q Increased V/Q Decreased V/Q

Figure 28.3 Pathophysiological mechanisms of V/Q mismatch.
hypoxaemic pulmonary vasoconstriction, which diffusability and the solubility of the gases. Conditions
results in reduced perfusion to those areas of the lungs that can cause diffusion abnormalities include end
which are poorly ventilated. stage pulmonary fibrosis or fibroproliferative acute
respiratory distress syndrome (ARDS).
Shunt
There are two types of shunts that may cause signifi-
Increased Venous Admixture
cant hypoxaemia: intrapulmonary and intracardiac. Low oxygen content returning to the pulmonary cir-
Intracardiac shunts include such aetiologies as culation can be a cause of hypoxaemia. This is often
a patent foramen ovale or an atrial septal defect. in the context of poor cardiac function or very high
These shunts will cause hypoxaemia as venous blood tissue consumption and extraction of oxygen. When
bypasses the lungs and travels from the right side of this is suspected as a primary cause of hypoxaemia,
the heart directly to the systemic side. detailed evaluation of cardiac function is required.
Intrapulmonary shunt is an extreme V/Q mis-
match where there is no ventilation of the associated Hypercarbic Respiratory Failure
lung unit despite being fully perfused. The most com- Hypercarbic respiratory failure, also known as type 2
mon cause of intrapulmonary shunt is atelectasis, respiratory failure or acute ventilatory failure, results
and fluid filled alveoli due to cardiogenic or non- in a rise in PaCO2 above the patient’s baseline. In most
cardiogenic pulmonary oedema. In non- diseased patients the normal CO2 is between 35 and 40 mmHg.
states there is a small physiological degree of intrapul- CO2 production is matched by CO2 elimina-
monary shunt (up to 3% or the systemic cardiac out- tion in steady state conditions. Hypercarbia can
put), which is due to circulation from the Thebesian result from three major pathophysiological mecha-
and bronchial circulation. nisms: increased CO2 production, decreased tidal
Severe shunts (greater than 30% of systemic car- ventilation or increased dead space.
diac output) due to the lack of ventilation do not
respond to supplemental oxygen therapy. This can be Increased CO2 Production
used as a diagnostic feature when assessing a patient
This can occur in both physiological and disease state
suspected to have a shunt.
conditions such as exercise, fever, major trauma, sepsis
and hyperthyroid states. The compensatory response
Diffusion Abnormalities to an increase in CO2 production is to increase alve-
Diffusion of oxygen and CO2 across the alveolar- olar minute ventilation by increasing both tidal vol-
capillary membrane is an extremely efficient process. umes and respiratory rate, with the objective both of
The ability of gases to diffuse efficiently is dependent maintaining a normal CO2 and of preventing acido-
upon several key features of the capillary- alveolar sis. Patients who do not have the ability or reserve
membrane including its total surface area, thickness, to increase their alveolar minute ventilation (i.e.
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pre-
existing neuromuscular disease) can develop due to the significant morbidity and mortality asso-
hypercarbic respiratory failure. ciated with the diagnosis. By most recent estimates,
mortality for patients diagnosed with severe ARDS is
Decreased Tidal Ventilation over 40%.
The details of ARDS diagnosis and treatment will
Decreased tidal volume ventilation resulting in
be discussed in Chapter 44. However, an important
reduced alveolar ventilation can be caused by pathol-
part of the diagnosis of this condition is to exclude a
ogy anywhere from central or peripheral nervous
cardiogenic cause of pulmonary oedema.
system to the respiratory muscles, chest wall, pleural
space and parenchyma. Common conditions in the
ICU which may cause this include CNS depressant Pneumothorax
medications such as narcotics and intravenous seda- A pneumothorax is the accumulation of air within the
tion, brainstem strokes, neuromuscular disorders like pleural space. It is most often caused by an acquired
myasthenia gravis, critical illness neuropathy and defect in either the parietal or visceral pleura.
myopathy, circumferential chest burns with signifi- Pneumothoraces can be classified as either spontane-
cant eschar, rib fractures with a flail segment, airflow ous or non-spontaneous. Spontaneous pneumothora-
obstruction due to severe emphysema, and central ces are less common within the ICU in comparison to
sleep disordered breathing. non-spontaneous pneumothoraces.
Spontaneous pneumothoraces most often occur in
Increased Dead Space healthy young adults. Certain risk factors can increase
the risk of a spontaneous pneumothorax such as
Increased dead space results from disease processes
underlying lung disease (i.e. emphysema), familial
that increase areas of the lung that do not participate
history, drug abuse or more rare causes such as cata-
in gas exchange, despite being ventilated. Dead space
menial pneumothorax.
can be both anatomical and alveolar.
Most pneumothoraces that are encountered in the
Anatomical dead space comprises the trachea,
ICU are not spontaneous and are trauma induced or
main bronchi and the conducting airways that do
iatrogenic. Iatrogenic pneumothoraces can be due to
not participate in gas exchange. An average adult has
barotrauma from mechanical ventilation, or they can
approximately 150 ml of anatomical dead space. In
be procedure related (such as central venous catheter
mechanically ventilated patients this is also increased
insertion, thoracentesis, transbronchial lung biopsy,
due to the ventilator circuitry, endotracheal tube and
percutaneous tracheostomy).
heat-moisture exchanger. Tracheostomy can signifi-
Mechanical ventilation induced pneumothoraces
cantly reduce the amount of anatomical dead space in
are often the result of barotrauma. Tissue disruption
comparison to an endotracheal tube.
allows the passage of air along the bronchovascular
Alveolar dead space results when non-perfused
bundle back to the hilum and into the pleural and
alveoli are ventilated. This is often the sequelae of
pericardial spaces, as well as into other interstitial tis-
disease processes such as chronic obstructive pulmo-
sues such as subcutaneous chest, neck and abdominal
nary disease, pulmonary emboli or fibroproliferative
tissues. Insufficient decompression via one of these
ARDS.
routes can lead to rupture of the pleural space and
subsequent pneumothorax.
Illustrative Clinical Scenarios in the ICU Clinically, a pneumothorax should be suspected
if a mechanically ventilated patient has an acute
Acute Respiratory Distress Syndrome increase in peak and plateau airway pressures. If the
Acute respiratory distress syndrome (ARDS) is char- pneumothorax is significant or causes obstruction
acterised by the acute onset of severe hypoxaemic res- to cardiac inflow or outflow via tension, there may
piratory failure with associated bilateral infiltrates on be associated hypotension. Hypoxaemia is com-
chest X-ray in the absence of significant left ventricu- mon as the pneumothorax results in collapse of the
lar dysfunction (see Table 28.1). Initially described in underlying lung. The chest X-ray can reveal a pneu-
1967 in a series of 12 patients, ARDS has been the sub- mothorax with evidence of a visceral pleural line
ject of significant clinical and research investigation and no lung markings beyond this. Radiography
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Table 28.1 Berlin definition of acute respiratory distress syndrome

Timing Within 1 week of known clinical insult or worsening respiratory symptoms
Chest X-ray Bilateral opacities (not due to effusions, collapse or nodules)
Origin of oedema Not primarily due to cardiac failure or fluid overload (use echo or pulmonary artery catheter)
Severity
Mild PaO2:FiO2 ratio 200–300 mmHg with PEEP/CPAP ≥ 5 cmH2O
Moderate PaO2:FiO2 ratio 100–300 mmHg with PEEP ≥ 5 cmH2O
Severe PaO2:FiO2 ratio < 100 mmHg with PEEP ≥ 5 cmH2O
in the upright position and at end expiration may • Increased afterload: Left ventricular outflow
improve the successful diagnosis of pneumothorax tract obstruction (systolic anterior mitral
by chest X-ray. Patients with a pneumothorax may leaflet prolapsing in the left ventricular outflow
have chest X-rays supine and as a result pleural air following mitral valve repair); tamponade;
rises to the anterior costophrenic sulcus resulting in severe vasoconstriction; peripheral VA ECMO
a deep visible costophrenic angle and double dia- counterflow in the descending aorta.
phragm, known as a deep sulcus sign.
In each case of pulmonary oedema the main cause
Treatment of pneumothorax varies depending on
needs to be identified and treated. However, basic
the severity and may include expectant management,
principles for all patients include oxygenation, main-
supplemental high concentration oxygen, aspiration
tenance of adequate perfusion and patient comfort.
and tube thoracostomy. High concentration supple-
The timing and magnitude of response are variable.
mental oxygen increases the rate of pneumothorax
Some patients respond to a single dose diuretic, oth-
resolution. An increase in the partial pressure of oxy-
ers need CPAP or IPPV, and in some ECMO may be
gen in the pleural space results in a reduction in par-
required to stabilise the situation.
tial pressure of nitrogen in the pleural space. Oxygen
Congestive heart failure can lead to significant
is more readily absorbed and results in increased reab-
hypoxaemia via the development of pulmonary
sorption of pleural gas. In large or unresolving pneu-
oedema. It most often occurs in patients with left
mothoraces, tube thoracostomy can be performed
ventricular systolic dysfunction related to a history
either with a large bore chest tube, or via percutaneous
of myocardial infarction or diastolic dysfunction
small bore chest tube.
from hypertension. There are several other aetiolo-
gies of cardiogenic origin that may lead to pulmonary
Cardiogenic Pulmonary Oedema oedema, including inherited and acquired cardiomyo-
pathies, valvular abnormalities (such as severe mitral
Pulmonary oedema is a much more common cause
regurgitation or severe aortic stenosis) and long
for dyspnoea in the cardiothoracic ICU. The causes of
standing dysrhythmias.
pulmonary oedema can be multifactorial but involve
Diagnosis of cardiogenic pulmonary oedema can
three main categories:
be made in a variety of ways. Chest X-ray findings
• Increased preload: Increased circulatory volume include pleural effusions, peribronchial cuffing and
due to chronic conditions (congestive cardiac Kerley-B lines, as well as vascular redistribution.
failure); excessive fluid administration; position There may be evidence of cardiomegaly on the X-ray
allowing increased venous return; removal of a if the process is chronic. Serum B-type natriuretic
venous return obstruction. peptide (BNP) can be elevated; however, this can be
• Reduced left atrial emptying: Mitral stenosis; non-specific in ICU patients. Echocardiography can
change of sinus rhythm to atrial fibrillation; be used to assess cardiac function and rule out valvu-
worsening of mitral regurgitation (papillary lar abnormalities. Pulmonary artery catheters can be
muscle rupture); sudden onset of severe AR; diagnostic as an elevated pulmonary capillary wedge
cardiogenic shock; severe bradycardia (complete pressure suggests elevated filling pressures and likely
heart block); diastolic heart failure. venous capillary hypertension.
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Cardiogenic pulmonary oedema, due to its hydro- compliance that can result in significant alveolar col-
static aetiology, is amenable to treatment with posi- lapse, which can also contribute to intrapulmonary
tive pressure ventilation (PPV). Application of either shunting. Bacterial pneumonias in particular can be
non-invasive positive pressure ventilation or intuba- associated with a hyperdynamic state, which can lead
tion and invasive mechanical ventilation can counter- to increased venous admixture.
act elevated venous pressures. Benefits of PPV include
reduction of both left and right ventricular preload as COPD
well as reduction of left ventricular afterload.
Exacerbations of chronic obstructive pulmonary dis-
ease (COPD) resulting in acute respiratory failure are
Pneumonia a common indication for admission to ICU. These
Pneumonia is a common aetiology for the develop- patients often present with hypercarbic respiratory
ment of hypoxaemic respiratory failure. For patients failure. COPD patients have either chronic bronchi-
admitted to hospital with a community acquired pneu- tis or emphysema as a dominant phenotype of their
monia (CAP), up to 20% may require ICU admission. disease. The primary issue in patients with COPD is
In one study in the UK, 6% of all ICU admissions were expiratory flow limitation. Several mechanisms are
due to pneumonia. responsible for this including impaired ciliary func-
Several risk factors can predispose patients to tion, excess mucus production and narrowing of the
develop CAP such as advanced age, chronic respira- peripheral airways, as well as decreased elastic recoil
tory insufficiency (e.g. COPD), smoking, alcohol from tissue destruction of the airway elastic support.
abuse, immunosuppression and multiple comorbid Chronic CO2 retention is due to the increase in dead
illnesses. space and reduction in alveolar minute ventilation.
The most common aetiologies for CAP include Patients often have clinical signs of hyperinflation
the bacteria Streptococcus pneumoniae, Haemophilus and airway obstruction including pursed lip breath-
influenzae, Klebsiella pneumoniae, Chlamydia pneu- ing, presence of a barrel chest and the use of accessory
moniae, and the viruses influenza A/ B, adenovi- respiratory muscles such as intercostals.
rus, respiratory syncytial virus, and parainfluenza. Acute exacerbations of COPD are commonly
Nosocomial pneumonias that develop while in hos- triggered by respiratory infections, usually viral in
pital (hospital acquired pneumonia) or whilst on nature. Other less common causes of acute exacer-
the ventilator (ventilator associated pneumonia) are bations include bacterial community acquired pneu-
more commonly caused by Gram-negative bacteria monias, environmental exposures or medication
such as Pseudomonas aeruginosa, Acinetobacter spp., non-compliance.
and Enterobacteriaceae spp., as well as Gram-posi- During an acute exacerbation, expiratory airflow
tive bacteria such as Staphylococcus aureus. Antibiotic obstruction is worsened by increased mucus produc-
resistance is much more common with nosoco- tion and bronchoconstriction. This leads to worsening
mial pneumonias as Gram-negative bacilli are often hyperinflation and reduced alveolar minute ventila-
extended spectrum beta lactamase producing and tion, ultimately resulting in a rise in CO2 and a res-
Staphylococcus aureus is methicillin resistant (MRSA). piratory acidosis. Concomitant hypoxaemia is often
Sputum and blood cultures can aid in stepping related to reduced alveolar minute ventilation and not
down antibiotics based on sensitivities. Chest X-ray V/Q mismatch.
findings of a lobar pneumonia include silhouetting of In addition to standard medical management of
the diaphragm or heart borders without signs of asso- acute exacerbations with bronchodilators, steroids
ciated volume loss (silhouette sign). In addition, air and antibiotics, non-invasive positive pressure venti-
bronchograms are highly suggestive of a consolidative lation is an important therapeutic option to consider,
process. as it can significantly reduce the work of breathing. By
There are several pathophysiological mecha- allowing the respiratory muscles to rest, it improves
nisms associated with pneumonia that cause hypox- alveolar minute ventilation and reduces hyperinfla-
aemia. Secretions and inflammatory infiltrates can tion. With less hyperinflation, the diaphragm can
lead to both shunt physiology as well as V/Q mis- restore its normal conformation and operate at a more
match. Progressively consolidated lungs have poor favourable position on the length-tension relationship
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curve. Clinical benefits of NIPPV use in COPD ischaemia, and haemodynamic instability. Details of
include potentially reducing nosocomial infections, NIPPV are discussed in Chapter 17.
ICU length of stay and mortality, as well as rates of
primary intubation. Endotracheal Intubation with Mechanical
Treatment of Acute Respiratory Failure Ventilation
Several strategies can be used to improve oxygena- In patients for whom supplemental oxygen techniques
tion and help CO2 clearance. Most importantly, the are insufficient and for whom NIPPV has failed or is
primary pathological process driving respiratory fail- contraindicated, endotracheal intubation and invasive
ure must be addressed and treated appropriately. For mechanical ventilation is an important therapeutic
example, pneumonia must be treated with appropri- option.
ate empirical antibiotics, or heart failure treated with There are several ways in which invasive mechani-
inotropes and diuretics. In addition to this several cal ventilation can improve oxygenation. High
adjunctive strategies can be used. inspired fractions of oxygen can be delivered directly
to the lungs. The ventilator allows a much more
sophisticated manipulation of the respiratory cycle.
Supplemental Oxygen The primary determinant of oxygenation is the mean
Supplemental oxygen delivered via nasal cannula or airway pressure (mean Paw) and significant manipu-
facemask is very simple to apply to patients, and is lation of the mean Paw can be accomplished while
a good starting point for mild to moderate hypox- on the ventilator. By increasing the inspiratory cycle
aemia. More recently, high flow humidified oxygen length time, the inspiratory pressure or the pulmonary
has become more readily available, and offers certain end-expiratory pressure (PEEP), the mean Paw can be
advantageous features. High flow humidified oxygen elevated to improve oxygenation. In order to avoid
can deliver high concentrations of oxygen without damaging the lungs further, however, a lung protec-
the need for intubation. In addition the heated air tive ventilation strategy which limits both volume and
improves secretion mobilisation. The high rates of pressure should be applied. Appropriate application of
oxygen flow can also provide a small amount of posi- PEEP to optimise compliance and/or oxygenation will
tive end-expiratory pressure (PEEP) that may help also prevent the development of atelectrauma. Details
improve atelectasis and shunt. of endotracheal intubation with mechanical ventila-
tion are discussed in Chapter 17.
Non-invasive Positive Pressure Ventilation
(NIPPV) Prone Positioning
There are two common indications for the use of Prone positioning of a patient with severe hypoxae-
NIPPV including pulmonary oedema causing hypox- mic respiratory failure has been shown to improve
aemic respiratory failure and acute exacerbations of oxygenation and also to potentially reduce mortality.
COPD leading to hypercarbic respiratory failure. For The primary mechanism for improvement of oxygen-
pulmonary oedema the use of continuous positive ation is improved V/Q matching and reduced shunt.
airway pressure (CPAP) is sufficient to reduce right In the supine position, dependent lung zones that are
and left ventricular preload as well as left ventricular well perfused do not ventilate well due to atelectasis
afterload, which can result in improvement in hypox- from lung injury, secretions and the weight of the
aemia. Patients with COPD induced hypercarbic res- heart. Dorsal lung segments benefit from increased
piratory failure should be treated with bilevel positive perfusion in the prone position. In addition, secretion
airway pressure (BIPAP). This will provide assistance clearance is improved while in the prone position.
in both oxygenation and ventilation.
General contraindications to the use of NIPPV Inhaled Pulmonary Vasodilators
include decreased level of consciousness due to rea- The use of inhaled pulmonary vasodilators, such as
sons other than CO2 narcosis, inability to clear secre- inhaled nitric oxide and prostaglandins, can improve
tions, recent facial trauma or surgery precluding the oxygenation. Despite an improvement in oxygena-
application of an oronasal mask, active myocardial tion, no studies to date have shown a definitive mor-
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tality benefit. The primary mechanism through which

oxygenation is improved is by better V/Q matching.
Further Reading
Ashbaugh DG, Bigelow DB, Petty TL, et al. Acute
respiratory distress in adults. Lancet. 1967; 2: 319–323.
Restrictive Fluid Strategy Force ADT, Ranieri VM, Rubenfeld GD, et al. Acute
In many conditions such as sepsis, trauma or pan- respiratory distress syndrome: the Berlin definition.
creatitis it is very easy to acquire a significant positive Journal of the American Medical Association. 2012;
fluid balance during the process of being resuscitated. 307: 2526–2533.
Studies demonstrating a restrictive fluid strategy Girou E, Schortgen F, Delclaux C, et al. Association of
approach have shown a reduced duration of mechani- noninvasive ventilation with nosocomial infections
cal ventilation. and survival in critically ill patients. Journal of the
American Medical Association. 2000; 284: 2361–1267.
Extracorporeal Membrane Oxygenation Keenan SP, Sinuff T, Burns KE, et al. Clinical practice
guidelines for the use of noninvasive positive-pressure
Extracorporeal membrane oxygenation can poten- ventilation and noninvasive continuous positive airway
tially be considered should all other less invasive pressure in the acute care setting. Canadian Medical
methods of improving oxygenation and CO2 clearance Association Journal. 2011; 183: E195–E214.
fail. This is reviewed in detail in Chapter 24. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and
outcomes of acute lung injury. New England Journal of
Medicine. 2005; 353: 1685–1693.
Learning Points Slutsky AS, Ranieri VM. Ventilator-induced lung
• There are two major types of respiratory injury. New England Journal of Medicine. 2013;
failure: hypoxaemic and hypercarbic. 369: 2126–2136.
• Hypoxaemic respiratory failure can be caused by The Acute Respiratory Distress Syndrome Network.
five mechanisms: low alveolar oxygen, V/Q Ventilation with lower tidal volumes as compared with
mismatch, shunt, diffusion impairment and traditional tidal volumes for acute lung injury and
increased venous admixture. the acute respiratory distress syndrome. New England
• Hypercarbic respiratory failure can be caused by Journal of Medicine. 2000; 342: 1301–1308.
three mechanisms: reduced alveolar ventilation, Vincent JL, Akca S, De Mendonca A, et al. The
increased dead space and increased CO2 epidemiology of acute respiratory failure in critically ill
patients. Chest. 2002; 121: 1602–1609.
production.
• V/Q mismatch is the most common mechanism Ware LB, Matthay MA. Clinical practice. Acute pulmonary
edema. New England Journal of Medicine. 2005;
of hypoxaemia within the ICU.
353: 2788–2796.
• Using the correct therapy for the underlying
Woodhead M, Welch CA, Harrison DA, et al.
aetiology of respiratory failure is crucial. For
Community-acquired pneumonia on the intensive
example, NIV is very efficacious for care unit: secondary analysis of 17,869 cases in the
exacerbations of COPD and cardiogenic ICNARC Case Mix Programme Database. Critical
pulmonary oedema. Care. 2006; 10(Suppl 2): S1.
MCQs
1. A 78 year old female is currently postoperative day (a) 10
1 following an elective cholecystectomy. Her pain (b) 17
control following surgery has been poor and she was
(c) 20
getting regular intravenous morphine. She develops
progressive hypoxaemia and an arterial blood gas is (d) 29
performed on room air. The results are as follows: pH
2. In the previous question the most likely cause of her
7.20, PaCO2 75 mmHg and PaO2 46 mmHg. Assume
hypoxaemia is:
she is at sea level (atmospheric pressure 760 mmHg).
Based on this arterial blood gas her A–a gradient is: (a) Hypoventilation
14:48:43
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(b) V/Q mismatch (b) Hypoxaemic respiratory failure due to cardiogenic

(c) Shunt pulmonary oedema
(d) Diffusion abnormality (c) Somnolence due to hypercarbia
3. Which of the following clinical scenarios does not (d) Poor secretion clearance
meet the Berlin criteria for ARDS? 5. Which of the following statements about pneumotho-
(a) 5 day history of bilateral pneumonia with P/F ratio races is correct?
of 250 while intubated and on mechanical ventila- (a) The presence of a deep sulcus sign on chest X-ray
tion with PEEP of 10 cmH20. will rule out a pneumothorax
(b) 5 day history of bilateral pneumonia with P/F ratio (b) Barotrauma induced pneumothoraces are the result
of 250 while on non-invasive positive pressure ven- of air travelling along the bronchovascular bundle
tilation with CPAP of 5 cmH20. towards the hilum
(c) 5 day history of unilateral pneumonia with P/F (c) Most pneumothoraces in the intensive care unit are
ratio of 100 while intubated and on mechanical spontaneous
ventilation with PEEP of 10 cmH20. (d) Small bore percutaneous chest tubes should not be
(d) 5 day history of bilateral opacities following aspira- used to drain pneumothoraces
tion with P/F ratio of 100 while intubated and on
mechanical ventilation with PEEP 10 cmH20.
4. Which of the following is a contraindication to the use
of non-invasive positive pressure ventilation?
(a) Hypercarbic respiratory failure due to COPD
exacerbation
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Shock in the Cardiothoracic Intensive

Chapter
29 Care Unit
Fabio Guarracino and Rubia Baldassarri
Definition Obstructive Shock
Shock may be defined as acute circulatory failure The main cause of circulatory failure is obstruction
characterised by inadequate tissue perfusion and cel- of circulation, as occurs in pulmonary embolism,
lular damage. The inability of the circulatory system pneumothorax and cardiac tamponade. Mechanical
to deliver adequate quantities of oxygen to meet cel- obstructions of ventricular ejection render the heart
lular demand is called cellular dysoxia. Therefore, the unable to pump adequate stroke volume (SV), result-
pathophysiological feature of shock is the imbalance ing in low CO and tissue hypoperfusion.
between oxygen delivery (DO2) and cellular oxygen Despite the different underlying pathophysiologi-
consumption (VO2). cal mechanisms, in each of these three shock states
(hypovolaemic, cardiogenic and obstructive), blood
Pathophysiology flow is significantly decreased, and oxygen delivery to
It should be considered that although the mismatch peripheral tissues by the circulation is surpassed by
between oxygen supply and demand is the main cellular oxygen consumption.
pathophysiological determinant of shock, the acute
circulatory decompensation responsible for the Distributive Shock
altered perfusion of shock can be induced by four Loss of vascular tone and consequent reductions
main mechanisms. in systemic vascular resistance (SVR) alter the dis-
Circulatory insufficiency in shock can result from tribution of blood flow, as in severe sepsis, major
one or a combination of these mechanisms, leading to trauma and anaphylaxis. In this pattern of shock,
four main patterns of shock: hypovolaemic, cardio- the cause of circulatory failure is misdistribution of
genic, obstructive and distributive shock. blood flow.
The macrocirculation is defined at a haemody-
Hypovolaemic Shock namic level in terms of CO and DO2, where, at stable
Acute loss of circulating volume (haemorrhage, concentrations of haemoglobin, CO is the main deter-
loss of fluids) reduces venous return, which leads minant of DO2.
to severe hypovolaemia and consequent circulatory The microcirculation regulates blood flow and cel-
impairment. lular oxygen supply according to cellular metabolic
requests. This regulation consists of increased tissue
Cardiogenic Shock perfusion and increased cellular metabolism, which
Acute cardiac failure, as occurs in acute myocardial occur in response to long-term signals from cells under
infarction, myocardial ischaemia, cardiomyopathies different metabolic conditions. Microcirculatory dys-
and arrhythmias, is the main cause of cardiogenic function is responsible for tissue damage and organ
shock. Dysfunction of heart pumping leads to low failure despite adequate systemic blood flow and opti-
cardiac output (CO) and circulatory failure. Although misation of the macrocirculation.
the underlying mechanisms of hypovolaemic and car- In septic shock, the microcirculation is profoundly
diogenic shock are different, circulation is impaired, affected, and tissue perfusion is consequently altered.
and oxygen delivery is decreased, with consequent tis- Vasoplegia and vascular hyporeactivity are the most
sue hypoperfusion. important features of the haemodynamic impairment
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Chapter 29: Shock
of septic shock. The loss of control of vascular tone

seems to be related to an imbalance between vasodila-
Epidemiology
All types of shock can occur in critically ill patients
tors and vasoconstrictors and is associated with high
admitted to the cardiothoracic intensive care unit
mortality rates. The loss of vascular tone is induced
(CT ICU), and two or more patterns of shock may be
by inflammatory mediators and endogenous vasodi-
present in the same patient. It is not uncommon for
latory mediators produced by cells under oxidative
cardiogenic shock to be complicated by septic shock,
stress conditions and increased metabolic activity.
and cardiogenic shock can complicate pre-existing
Markers of both systemic inflammation and cellular
septic shock. It should be considered that haemody-
oxidative metabolism (pCO2, lactate, K+, H+, nitric
namic instability is one of the most common causes of
oxide (NO), prostaglandins, interleukin- 1, adeno-
admission to the ICU.
sine, inorganic phosphate) can be commonly detected
in patients with altered cardiovascular function and
shock. The actions of these products result in endothe- Diagnosis
lial dysfunction and altered microvascular perfusion. Circulatory shock is commonly associated with
The altered modulation between vasodilating and haemodynamic instability characterised by moder-
vasocostricting agents is responsible for vasoplegia ate to severe arterial hypotension and signs of tissue
and for hyporeactivity of arterial vessels to vasocon- hypoperfusion. Arterial hypotension, which is defined
striction, which is common in septic shock patients. as a systolic blood pressure less than 90 mmHg,
The predictive value of these mediators as biomarkers a mean arterial pressure (MAP) <65 mmHg, or a
is lower than that of the concentration of plasma lac- decrease ≥40 mmHg from baseline, is commonly pre-
tate; therefore, their routine use as biomarkers is not sent in patients with shock. However, hypotension is
recommended. not required to diagnose shock, as recently empha-
sised by the revision of the recommendations of the
2006 guidelines for the management of patients with
Ventriculoarterial (VA) Coupling shock. Signs of peripheral hypoperfusion are more
VA coupling reflects the interaction between cardiac suggestive in the diagnostic evaluation of shock, along
function and the vascular system. When the two com- with increased plasma levels of lactate and decreased
ponents of the cardiovascular system, the heart and central oxygen saturation. The three sites that can
the arterial tree, are coupled, maximal efficiency is be easily evaluated and most commonly reveal tis-
achieved. VA coupling can be defined as the ratio of sue hypoperfusion are the skin, kidneys and brain
arterial elastance (Ea) to ventricular elastance (Ees) (Table 29.1). Patients with cardiovascular impairment
(Ea/Ees), as proposed by Suga in 1969. When the heart generally present with non-specific symptoms, such
pumps a quantity of blood that matches the capability as moderate to severe arterial hypotension associated
of the arteries to receive it, the system is optimised. with clinical signs of tissue hypoperfusion, such as
Under different physiological and pathological condi- increased concentrations of blood lactate, decreased
tions, the heart provides adequate flow and pressure central venous oxygen saturation (ScvO2), reduced
to ensure tissue perfusion. The arterial system adapts urine output, cold skin and neurological symptoms,
to match the continuous variations in blood flow. VA such as mental confusion or agitation. As recently
decoupling occurs in most acute altered haemody- reported in the literature, hyperlactataemia is so
namic states. This means that cardiovascular function strongly associated with shock that it is assumed to be
is impaired and that global perfusion is suboptimal. part of the definition of shock. Increased blood con-
Both increased and decreased arterial tone negatively centrations of lactate above the cut-off of 2 mEq/l rep-
affect VA coupling in shock. Loss of vascular tone resent severe metabolic alterations due to inadequate
due to septic shock and vasoconstriction imposed by utilisation of oxygen carried to cells via the circulation
either autoregulatory mechanisms induced by hypo- (DO2/VO2 mismatch). Although lactate levels can also
tension or the use of vasopressors are the main causes increase with normal tissue perfusion and adequate
of changes in Ea. Ees can be decreased by alterations oxygenation, in most cases, especially in cases of acute
in LV contractility, which occurs in both cardiogenic circulatory failure, hyperlactataemia is associated
shock and septic shock when myocardial depression with cellular dysfunction, and it negatively affects the
occurs. outcomes of patients with all types of shock. Recently,
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Table 29.1 Signs of systemic hypoperfusion at three levels systemic blood pressure levels; when blood pressure
Skin Inspection Cold falls below the limits of autoregulation, haemody-
Pale namic instability manifests, and cellular injury occurs.
Mottled Ultimately, the mismatch between DO2 and VO2
Cyanotic results from an imbalance between the macrocircula-
Slow capillary refill time tion and microcirculation.
Kidney Urine output ≤0.5 ml/kg/hr Patients with cardiogenic shock should be further
Brain Mental status Obtunded investigated with respect to cardiac function, and the
Disorientation use of inotropes is recommended to improve contrac-
Confusion tility and SV in severe heart dysfunction.
The use of vasopressors is indicated in cases of
insufficient responsiveness to fluid administration.
lactate-guided therapy was proposed for patients with
shock. Some authors have reported that this reduces
hospital mortality by 20% every 2 hours for the first 8
Monitoring Cardiac Function
hours of therapy. Plasma lactate levels should be rou- and Haemodynamics in Patients
tinely evaluated in patients exhibiting acute haemody-
namic changes to assess peripheral organ perfusion;
with Shock
Cardiac function should be accurately evaluated in
lactate values can also be helpful in determining the
cases of acute circulatory dysfunction to define the
effectiveness of therapeutic strategies as normalisa-
type of shock, first distinguishing among cardiogenic,
tion of plasma lactate concentrations is correlated
hypovolaemic and obstructive shock, which are all
with improvements in tissue perfusion.
characterised by low CO. In addition, in patients with
ScvO2 may reflect DO2/VO2 mismatches in acute
suspected septic shock, investigations of cardiac perfor-
circulatory failure. Low ScvO2 (<70%) is assumed to
mance may provide information about global haemo-
reflect inadequate oxygen delivery to peripheral tis-
dynamic impairment and the eventual myocardial
sues. Nevertheless, normal or even high values of
depression that frequently complicates septic shock.
ScvO2 do not seem to be correlated with adequate
Advanced haemodynamic monitoring may be
oxygen transport.
required in patients with severe cardiovascular insta-
Another indicator of adequate blood flow and tis-
bility either to categorise shock or to evaluate respon-
sue perfusion is the venoarterial carbon dioxide dif-
siveness to therapy.
ference (pCO2 gap), the difference between central or
In this context, echocardiography has been recog-
mixed venous carbon dioxide partial pressure (pCO2)
nised as the most useful tool to either evaluate car-
and arterial pCO2. A value ≥6 mmHg indicates low
diac function or allow haemodynamic assessments
peripheral perfusion despite normal ScvO2 levels.
in patients with shock. Echocardiography is a non-
It should be considered that some patients have
invasive and reliable bedside method of detecting
normal systolic blood pressure despite evident car-
cardiac function, CO and preload in acute circula-
diovascular decompensation because of activation of
tory decompensation or in follow-up of patients with
compensatory mechanisms of autoregulation. Arterial
shock. Assessment of cardiac function is also recom-
vasoconstriction is the primary mechanism of imme-
mended to determine either therapeutic strategies or
diate compensation in cases of circulatory failure.
the need for adjunctive haemodynamic monitoring.
Increased SVR induced by arterial vasoconstriction
The main limitation of echocardiography is that it
allows systemic blood pressure to be maintained
cannot be continuously performed; therefore, haemo-
within a normal range, even in cases of large volume
dynamic monitoring should be performed in criti-
loss or severe cardiac dysfunction. This autoregulation
cal patients for whom continuous information about
mechanism also counteracts the loss of vascular tone,
haemodynamics is required.
which is present in maldistributive shock, ensuring
normal arterial blood pressure in the early phase of
cardiovascular decompensation. Fluid Responsiveness
Autoregulation mechanisms ensure adequate For these reasons, therapeutic interventions to restore
blood flow and DO2 to tissues and organs at different adequate circulation and global perfusion should be
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Chapter 29: Shock
Table 29.2 Static and dynamic methods for the evaluation of fluid responsiveness
Static methods Pressures • Central venous pressure (CVP)
• Pulmonary artery occlusion pressure (PAOP)
Areas and volumes • Left ventricular end diastolic area (LVEDA)
• Left ventricular end diastolic volumes (LVEDV)
Diameters • Inferior vena cava (IVC)
Dynamic methods • Systolic pressure variation (SPV)
• Pulse pressure variation (PPV)
• Stroke volume variation (SVV)
• IVC respiratory variation
• Subaortic velocity time integral (VTI) variation
• SVC respiratory variation
• Internal jugular vein (IJV) and subclavian vein respiratory variation
• Aortic velocity variation
• Carotid artery peak velocity variation
based on preload, afterload and cardiac function. between the heart and lungs in patients under positive
Although fluid resuscitation is the first line therapy pressure mechanical ventilation (MV). The effects of
in patients with shock, the risks associated with positive pressure ventilation on RV ventricle preload
unnecessary fluid administration have recently been and afterload have been well demonstrated. During
demonstrated. In this context, in cases of acute cir- the respiratory cycle, RV preload decreases (reduc-
culatory failure, appropriate fluid administration and tion in the venous return), and RV afterload increases
the response of the patient to an increased preload because of an increase in transpulmonary pressure.
should be adequately investigated. The role of fluid The decrease in RV preload negatively affects LV fill-
responsiveness (FR) as a guide for fluid resuscitation ing and LV SV. The changes induced on LV SV by
in shock has been progressively emphasised. FR rep- positive pressure ventilation and arterial pulse pres-
resents the ability of the left ventricle to increase SV sure can be used to detect FR.
after administration of fluids. An increase of 15% in Dynamic measures of preload in patients with
SV or CO after administration of a bolus of fluid indi- acute circulatory decompensation have been increas-
cates the so-called fluid response. FR can be evaluated ingly used in recent years because they have been
either by static or by dynamic methods, as reported in recognised as accurate and reliable. These methods
Table 29.2. Although central venous pressure (CVP) evaluate the dynamic response to fluid administration
and pulmonary artery occlusion pressure (PAOP) by measuring variations in LV SV. Several methods
are commonly employed to assess left ventricle (LV) to assess FR with dynamic measurements have been
and right ventricle (RV) preload, respectively, their proposed in recent years. Evaluations of changes in
prognostic value is poor. Measurements of cardiac internal jugular venous (IJV) pressures, as assessed
chamber area and volumes detected by echocardio- by echocardiographic measures of changes in IJV
graphic assessments and the thermodilution method diameter, have also been reported to be effective in FR
are good indicators of preload but have poor prog- detection.
nostic value. The static diameter of the inferior vena
cava (IVC) has been proposed as an index of volae-
mia because it is reduced in hypovolaemic patients. Echocardiography
Its use is not recommended in the detection of FR. In cases of shock, evaluation of the haemodynamic
While static measures indicate preload with more or profile in terms of CO, LV filling pressure and
less accuracy, depending on the method employed, flow is fundamental to defining the type of shock
dynamic measures evaluate the ability of the LV to and to assessing the adequacy of therapy. Because
increase preload after fluid administration. Dynamic cardiovascular impairment may be due to differ-
measures are based on the physiological interaction ent underlying mechanisms, the availability of a
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diagnostic instrument that allows complete assess- Echocardiography allows evaluation of RV mor-
ments of haemodynamic variables in shock is of phology and performance with regard to the interac-
paramount importance. In this context, echocardio tion between the LV and RV. In cases of obstructive
graphy has been largely recognised as the best dia shock, when pulmonary embolism or cardiac tam-
gnostic tool in acute altered haemodynamic states. ponade occur, direct visualisation of a dilated RV as
Echocardiographic examinations allow direct visuali- well as of the loss of the normal shape of the inter-
sation of the heart and cardiac structures that support ventricular septum are good indicators of increased
the diagnoses of different types of shock. In addition pulmonary vascular resistance.
to its well-known ability to investigate both LV and RV In this context, non-invasive evaluations of ven-
function, echocardiography allows estimation of the tricular and arterial elastances allow detailed patho-
most useful haemodynamic parameters to categorise physiological assessments of patients with shock,
the haemodynamic profile of shock. Application of which promotes tailoring of treatments for VA uncou-
various echocardiographic techniques (two-dimen- pling profiles.
sional imaging, Doppler and colour-Doppler, tissue
Doppler and, more recently, three-dimensional echo- Therapeutic Strategies
cardiography) permits the study of myocardial con- Restoration of adequate circulation and optimisation
tractility and cardiac performance. Evaluation of the of tissue perfusion are the goals of therapeutic man-
haemodynamic profile of shock is primarily achieved agement in all pathophysiological patterns of shock.
via evaluations of SV and CO. Application of pulse It should be considered that there is no evi-
wave Doppler at the level of the mitral valve allows dence of an optimal value of arterial blood pressure.
evaluations of transmitral flow. The two peak veloci- Therefore, an individualised approach is recom-
ties of diastolic flow through the mitral valve are the mended, even if a mean arterial pressure ≥65 mmHg
E wave (early filling) and A wave (atrial contraction). is considered sufficient to maintain adequate tissue
The E/A ratio is a good index of LV diastolic function. perfusion in most cases. It should be kept in mind
The use of tissue Doppler imaging at the level of the that patients suffering from arterial hypertension
annulus of the mitral valve measures early diastolic may require higher levels of systemic pressure to
mitral annular peak velocity (E’). E/E’ has been con- ensure organ perfusion.
sidered the best echocardiographic index of LV fill- However, although early therapeutic strategies
ing pressure and is a preload-independent measure can be applied in all patients with haemodynamic
of diastolic function. Although values of E/E’ < 8 and instability and circulatory failure, early diagnosis of
>15 are suggestive of low and high filling pressures, the specific type of shock is strongly recommended
respectively, it should be considered that calculation for targeting therapeutic interventions. Although
of this ratio (E/E’) provides semiquantitative esti- the diagnosis of shock is easily achieved via clinical
mations of intracardiac filling pressure and that in examination, differentiating among the various types
a range between 8 and 15, LV filling pressure is not of shock (Table 29.3) is neither simple nor immedi-
necessarily adequate. ate in most cases. Arterial hypotension is commonly
Table 29.3 Variation of haemodynamic parameters in the different patterns of shock
Type of shock HR BP CVP PAP PAOP CO ScvO2 SVR PVR

Hypovolaemic ⇧ ⇩ ⇩ ⇩ ⇩ ⇩ ⇩ ⇧ ⇧
Cardiogenic ⇧ ⇩ ⇧ ⇧ ⇧ ⇩ ⇩ ⇧ ⇧
Obstructive ⇧ ⇩ ⇧ = ⇧⇩ = ⇧⇩ ⇩ ⇩ ⇩ ⇧
Distributive ⇧ ⇩ ⇧ = ⇧⇩ ⇩ = ⇧⇩ = ⇧⇩ ⇩ =⇧
HR heart rate; BP blood pressure; CVP central venous pressure; PAP pulmonary artery pressure; PAOP pulmonary artery occlusion
pressure; CO cardiac output; ScvO2 central venous oxygen saturation; SVR systemic vascular resistances; PVR pulmonary vascular
resistances.
⇧ increased; ⇩ decreased; = no change.
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Chapter 29: Shock
present in hypovolaemic shock, but normal or even macrocirculation or microcirculation impairment

higher values of arterial blood pressure can be found induces the cellular dysfunction and organ failure
in patients with cardiogenic shock. Low CO is the in shock.
main marker of cardiogenic and hypovolaemic shock, • Although arterial hypotension is commonly
while septic shock patients can have hyperkinetic present in the states of circulatory
circulation. Obstructive shock can result in systemic decompensation and despite it being the main
hypotension and high pulmonary pressures and intra- feature of the haemodynamic instability in shock,
cardiac filling pressures. Moreover, different patho- the presence of hypotension is not required to
physiological patterns of shock can coexist in the same make a diagnosis of shock. The signs of tissue
patient. For this reason, the diagnosis of the type of hypoperfusion are more suggestive for shock than
shock can be achieved only with an advanced haemo- arterial hypotension.
dynamic investigation. • Fluid resuscitation is the first intervention to
restore volaemia and to improve arterial blood
Conclusion pressure in the majority of the patients with septic
Shock is a complex, life threatening state in which shock and hypovolaemic shock.
tissue hypoperfusion and cellular injury induced by • The evaluation of the Ea/Ees ratio can be
acute circulatory insufficiency can lead to organ failure helpful for understanding the pathophysiology
and death. For this reason, restoring adequate tissue of altered haemodynamic states, and for
perfusion and DO2/VO2 balance is the primary objec- guiding therapy and testing the effectiveness of
tive of treatment. The role of the microcirculation, the treatments.
site at which effective oxygen exchange between cap- • The manipulation of the preload with fluid
illaries and cells occurs, has become a topic of inter- administration should be adequately monitored
est in recent years. Therapeutic strategies that target in the light of both diastolic and systolic function
restoration of normal microcirculatory efficiency have affecting the preload reserve. The increase of the
been proposed, although further investigations are preload can improve the CO and global perfusion
required. in the majority of patients with circulatory failure,
Because the peripheral organs have a different but not in all of them.
response to hypoxia and tissue damage can quickly
worsen, early diagnosis and immediate treatment are
mandatory in patients with shock. It should be con-
Further Reading
sidered that diagnosis of the type of shock is necessary Antonelli M, Levy M, Andrews PJ, et al. Hemodynamic
monitoring in shock and implications for
to provide adequate therapy, including the removal management. International Consensus Conference,
of the underlying cause, to ensure haemodynamic Paris, France, 27–28 April 2006. Intensive Care
stabilisation. It should be kept in mind that either Medicine. 2007; 33: 575–590.
inadequate or excessive therapy can be detrimental Aya HD, Carsetti A, Bazurro S, et al. From cardiac output
in shock. Haemodynamic monitoring is required to to blood flow auto-regulation in shock. Anaesthesiology
evaluate the haemodynamic profile of shock and to Intensive Therapy. 2015; 47: s56-s62.
assess the effectiveness of therapy. Echocardiography Cecconi M, De Backer D, Antonelli M, et al. Consensus
has been recognised as the best tool to investigate both on circulatory shock and hemodynamic monitoring.
cardiac function and haemodynamics, particularly Task force of the European Society of Intensive
ventricular and arterial elastances. Optimisation of Care Medicine. Intensive Care Medicine. 2014;
VA coupling may play a pivotal role in the therapeutic 40: 1795–1815.
approach to altered haemodynamic states. Guarracino F, Baldassarri R, Pinsky MR. Ventriculo-
arterial decoupling in acutely altered hemodynamic
states. Critical Care. 2013; 17: 213.
Learning Points Guarracino F, Bertini P. Use of echocardiography in
• Shock can be defined at a cellular level when the critically ill patients: the intensivist’s point of view.
circulation becomes unable to deliver sufficient Giornale Italiano di Cardiologia (Rome). 2015;
oxygen to meet the cellular demand. Either 16: 341–343.
14:49:26
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262
Guarracino F, Ferro B, Forfori F, et al. Jugular vein Sakr Y, Reinhart K, Vincent JL, et al. Does dopamine
distensibility predicts fluid responsiveness in septic administration in shock influence outcome? Results of
patients. Critical Care. 2014; 18: 647. the Sepsis Occurrence in Acutely Ill Patients (SOAP)
Pinsky MR. Both perfusion pressure and flow are Study. Critical Care Medicine. 2006; 34: 589–597.
essential for adequate resuscitation. Sepsis. 2000; Suga H. Time course of left ventricular pressure-volume
4: 143–146. relationship under various end-diastolic volume.
Japanese Heart Journal. 1969; 10: 509–515.
MCQs
1. What is shock? (c) Pulmonary capillary wedge pressure is necessary
(a) Shock is presented as a low blood pressure for diagnosis
(b) Shock is always a result of low cardiac output (d) Can be diagnosed clinically
(c) Shock is acute circulatory failure characterised by (e) High mixed venous oxygenation rules out
inadequate tissue perfusion and cellular damage cardiogenic shock
(d) Shock is always characterised by hypovolaemia 4. Treatment of shock:
(e) Shock is septic if it has high systemic vascular (a) Fluid bolus is always the first step
resistance (b) Reduction of preload is appropriate in
2. Cardiogenic shock: cardiogenic shock
(a) Is always a result of lower pump function (c) ADH is the first line treatment for anaphylaxis
(b) Hypoperfusion is not always present (d) Increasing cardiac output is a treatment strategy in
septic shock
(c) Hypotension is necessary for the diagnosis
(e) Fluid bolus is appropriate for cardiogenic shock
(d) Tachycardia is a necessary feature for diagnosis
(e) Often presents with high preload
3. Monitoring in cardiogenic shock:
(a) Patients must have arterial line for the diagnosis
(b) CVP measure is mandatory for diagnosis
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Systemic Hypertension in Cardiothoracic

Chapter
30 Critical Care
Antonio Rubino and Susan Stevenson
Introduction This simplification diminishes the contribution

of other haemodynamic variables. For example, the
Hypertension is a commonly encountered clinical
stroke volume depends on the contractility of the
problem in the cardiothoracic critical care unit in both
left ventricle which itself depends on multiple factors
its chronic and acute forms. It is estimated that over
including preload, afterload and sympathetic activa-
one billion of the world’s population are affected by
tion. Systemic vascular resistance is also influenced by
hypertension, many of whom may be undiagnosed or
the autonomic nervous system as well as precapillary
inadequately managed. Chronic hypertension is a risk
sphincter tone. Hypertension can occur acutely with
factor for cardiovascular disease and is therefore seen
an increase in any of the above variables.
with greater prevalence in the cardiothoracic patient
In chronic primary or essential hypertension,
population. Such patients are at greater risk of pre-
decreases in vascular compliance and endothelial cell
existing left ventricular dysfunction, cerebrovascular
dysfunction result in sustained elevations in blood
disease and chronic kidney disease, factors which
pressure, which generally develop slowly over time.
are independently associated with poorer outcomes.
This is accompanied by compensatory changes in
Acute hypertension in cardiothoracic critical care may
physiology which themselves have implications in
represent undiagnosed chronic hypertension or arise
managing chronically hypertensive patients on the
as a complication of the presenting complaint. Acute
cardiothoracic critical care unit.
hypertension can complicate cardiac surgery, leading
In health, acute changes or swings in mean arte-
to haemorrhage, end-organ damage, prolonged length
rial pressure are sensed by baroreceptors found in the
of stay and poorer outcomes.
carotid sinus and aortic arch. An increase in blood
pressure results in activation of a negative feedback
Aetiology and Pathophysiology reflex loop whereby both heart rate and systemic
The aetiology of hypertension in the cardiothoracic vascular resistance fall in response to increased para-
critical care unit is often multifactorial and may sympathetic tone. This results in a lowering of blood
resolve with management of the underlying precipi- pressure. In chronic hypertension baroreceptors reset
tant alone. Identification of the exact cause requires a over time to a higher level of mean arterial pressure,
systematic approach as seen in Table 30.1. a process which is reversed with initiation of anti-
Before initiation of anti-hypertensive therapy, an hypertensive therapy.
underlying cause should be sought and corrected. This Additionally, organ blood flow, which is main-
is particularly true in the case of raised intracranial tained at a near constant level by the process of
pressure whereby mean arterial pressure is raised in autoregulation, is also adjusted to a higher level of
order to maintain cerebral perfusion pressure. perfusion pressure. Autoregulation allows blood ves-
Blood pressure or mean arterial pressure (MAP) sels to adjust their calibre in response to metabolic,
is considered in simple terms as the product of the mechanical and neurogenic factors, and is particularly
cardiac output (CO) and systemic vascular resistance important in the maintenance of blood flow in cer-
(SVR). The cardiac output itself is determined by the ebral, coronary and renal perfusion. Mechanical fac-
product of the heart rate (HR) and stroke volume (SV) tors refer to changes in arterial pressure transmitted
and can be summarised as follows: transmurally. Increases in arterial pressure lead to the
MAP (mmHg) = (HR × SV) × SVR. compensatory response of vasoconstriction thereby
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Table 30.1 Aetiology of hypertension in the cardiothoracic critical care unit
System Cause
Central nervous system Cerebrovascular accident
Inadequate analgesia
Postoperative cognitive dysfunction or delirium
Raised intracranial pressure
Anxiety
Cardiovascular Preoperative hypertension
Alleviation of obstructed outflow with hypertrophied LV
Postbypass hypervolaemia
Inappropriate or excessive vasopressor or inotropic support
Respiratory Hypercapnia
Hypoxaemia
Renal Acute kidney injury
Urinary retention
Blocked urinary catheter
Other Hypoglycaemia
Acute alcohol or nicotine withdrawal
Steroids
Failure to reinitiate anti-hypertensive medication
preventing a sudden increase in flow. Autoregulation adequate ventricular relaxation and subsequent con-
protects from the deleterious effects of acute hypoper- gestive heart failure can supervene.
fusion or hyperperfusion. However, this only occurs
within a certain range of mean arterial pressures. The
lower range of the autoregulation curve varies mark-
Diagnosis
edly between individuals and depending on acute The diagnosis and management of hypertension must
care setting. Traditionally the lower limit is thought be taken in the context of its presentation. The spec-
to be 60 to 70 mmHg in most individuals. The upper trum of hypertension includes an incidental finding in
limit has never been clearly defined but it certainly is an asymptomatic patient to hypertensive crises with
<110 mmHg in many individuals. Outside this range, associated organ damage. In the context of the cardio-
blood vessels are either maximally dilated or con- thoracic unit this ranges from cautious reintroduction
stricted and flow therefore becomes directly depend- of preoperative anti- hypertensive medication post-
ent on perfusion pressure. In chronic hypertension, operatively to rapid lowering of blood pressure in the
the autoregulation curve is shifted to the right for a situation of aortic dissection to limit further extension
given mean arterial pressure as shown in Figure 30.1. of the false lumen.
This explains why organ ischaemia may occur with Preoperative hypertension is typically diagnosed
rapid lowering of mean arterial pressure in patients in the primary care setting through routine screening.
with established chronic hypertension. The traditional cut-off blood pressure is 140/90 mmHg
Chronic hypertension results in an increase in or more. The blood pressure must be measured in
afterload, which leads to an increase in myocardial both arms and replicated on two separate occasions.
work. Over time this is maintained or compensated Further confirmation requires ambulatory or home
for by ventricular hypertrophy. In terms of coronary blood pressure monitoring. Hypertension can be clas-
blood flow, unless the increase in demand can be sified based on the severity of blood pressure.
met by an increase in supply, ischaemia may occur. • Stage 1: Blood pressure of 140/90 mmHg or more
Additionally, chronically elevated mean arterial pres- AND an average blood pressure of 135/85 mmHg
sure can lead to diastolic dysfunction due to failure of or more on home or ambulatory monitoring.
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265
Chapter 30: Systemic Hypertension
process. This includes pathologies affecting the adre-

nal gland such as excess catecholamines as seen in
phaeochromocytoma and aldosterone in Conn’s syn-
Cerebral Blood Flow
drome. Secondary hypertension is more common in

the younger population and treatment targets the
underlying disease in addition to traditional anti-
hypertensive medication.
Acute hypertension can present in the critical care
setting, the emergency department or primary care.
Acute severe elevations in blood pressure are often
classified based on the presence or absence of end-
Cerebral Perfusion Pressure organ damage. End-organ damage has been quoted as
being present in 19% of all presentations of acute severe
hypertension. A hypertensive emergency describes
Normal
Chronic Hypotension when severe hypertension as defined by BP >180/110
Chronic Hypertension is associated with end-organ damage. Examples of
end-organ damage can be seen in Table 30.2. Under
Figure 30.1 Cerebral blood flow autoregulation curve. these circumstances, anti- hypertensive treatment
should be initiated as a priority in a monitored envi-
ronment. Severe hypertension in the absence of end-
• Stage 2: Blood pressure of 160/100 mmHg or organ damage is considered a hypertensive urgency.
more AND an average blood pressure of 150/ Treatment should be offered immediately but does
95 mmHg or more on home or ambulatory necessitate hospitalisation.
monitoring.
• Stage 3: Systolic blood pressure of ≥180 mmHg
OR diastolic blood pressure ≥110 mmHg.
Management
Whilst awaiting confirmation, further investigations Preoperative Management
looking for evidence of target organ damage should The guidelines for the management of chronic hyper-
be performed. This includes fundoscopy, biochemis- tension are outlined by NICE. Patients with hyperten-
try for renal function and lipid profile, urinary protein sion requiring cardiothoracic surgery should ideally
levels and an electrocardiograph. be established on effective anti-hypertensive therapy
Stage 3 hypertension is also referred to as severe in primary care. Current targets suggest an optimal
hypertension and is considered a hypertensive BP of below 140/90 mmHg in those aged less than
urgency. In these circumstances immediate initia- 80 years and below 150/90 mmHg in people aged over
tion of treatment should be considered. In addition
for patients with suspected accelerated hypertension,
defined as severe hypertension with signs on fundos-
copy of hypertensive retinopathy or papilloedema, a Table 30.2 System based examples of end-organ damage
referral for immediate specialist advice and treatment
System End-organ damage
should be made.
Hypertension can also be classified based on Central nervous system Cerebrovascular accident
its aetiology. Primary or essential hypertension Hypertensive encephalopathy
describes hypertension which occurs without an Hypertensive retinopathy
underlying identifiable cause. This represents over Cardiovascular Left ventricular hypertrophy
90% of all cases. It typically arises in the elderly. Heart failure
The exact aetiology is unclear but is likely to be an Myocardial ischaemia
interaction of environmental and genetic factors Aortic dissection
resulting in age-related decline in vessel compliance.
Renal Hypertensive nephropathy
Secondary hypertension on the other hand is hyper-
Respiratory Pulmonary oedema
tension as a consequence of an underlying disease
14:51:03
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266
80 years. Poorly managed or undiagnosed hyperten- hypertension and expert advice at this stage should be
sion should be identified at surgical pre-assessment sought.
and appropriate treatment instigated. No specific cut- Presently beta-blockers are not recommended as
off values exist above which surgery should be can- initial therapy for hypertension except in certain cir-
celled based on the presence of hypertension alone. cumstances such as women of child-bearing age and
For non-cardiac elective surgery, a blood pressure those intolerant of ACE inhibitors and ARBs. Extreme
above 180/110 mmHg would be an indication for can- caution should be exercised with all of these agents
cellation and optimisation of blood pressure control in patients with aortic stenosis, impaired ventricular
prior to surgery. function or pulmonary hypertension.
Initiation of anti-hypertensive therapy is indicated
in the following situations: Guidance on Pre-existing
• Stage 1 hypertension, less than 80 years of age and Anti-hypertensive Therapy in the
one of the following:
○○ Target organ damage Perioperative Period
○○ Any cardiovascular disease The nature of cardiac surgery dictates that optimal
○○ Renal disease blood pressure control should be ensured through-
○○ Diabetes out the perioperative and postoperative period. For
example, dehiscence of coronary grafts can result in
○○ Predicted 10 year cardiovascular risk of more
life threatening haemorrhage, cardiac tamponade,
than 20%.
return to theatre with resternotomy, use of blood
• Stage 1 and less than 40 years of age.
products and therefore potentially death. Patients
• Stage 2 or 3. on established therapy should therefore continue
The choice of treatment subsequently depends on age, up until the day of surgery unless specifically
ethnicity and response to treatment. This is outlined contraindicated.
in Table 30.3. Current practice advocates the continuation of
Before moving on to each step, compliance and both beta- blockers and calcium channel blockers
optimal dosing should be ensured before the addition on the day of surgery. Significant work has looked
of a further agent. Additionally, hypertension which specifically at the cardioprotective effects of beta-
persists despite triple therapy is considered resistant blockers in the perioperative period. Withdrawal of
beta-blockers on those taking them chronically is
Table 30.3 NICE recommendations for management of hypertension
Treatment Patient Recommended therapy

step
1 • Less than 55 years ACE inhibitor or
ARB
• Over 55 years CCB or
• Black people of African or Caribbean origin of any age thiazide-like diuretic
2 • Any patient not controlled on step 1 Combined ACE inhibitor and CCB
• Black people of African or Caribbean origin or any age not ARB (in preference to ACE inhibitor) combined with
controlled on step 1 CCB
3 • Any patient of any origin not controlled on step 2 Triple therapy: combination of ACE inhibitor or ARB
with CCB and diuretic therapy
4 • Any patient of any origin not controlled on step 3 and Addition of spironolactone to step 3 treatment
blood potassium level of 4.5 mmol/l or less
• Any patient of any origin not controlled on step 3 and High-dose diuretic therapy in addition to step 3
blood potassium level of more than 4.5 mmol/l treatment
ACE angiotensin converting enzyme, ARB angiotensin II receptor blocker, CCB calcium channel blocker.
14:51:03
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267
associated with significant adverse cardiac outcomes

and they should therefore be continued. Controversy
Postoperative Management
Any invasive surgery to the thorax is associated with
however exists over their introduction in the peri-
a significant acute phase response mediated by acti-
operative period due to evidence demonstrating
vation of the sympathetic nervous system and renin-
an increase in risk of stroke and all-cause mortal-
angiotensin-aldosterone system, both of which serve
ity despite a reduction in adverse cardiovascular
to promote an increase in cardiac output and therefore
outcomes.
tissue oxygen delivery but may in doing so increase
In the case of diuretics, including thiazides and
blood pressure. Hypertension is therefore a common
thiazide-like diuretics, concerns exist over the poten-
finding in the initial hyperdynamic postoperative
tial for diuretic induced volume depletion and electro-
period. Postoperative hypertension has previously
lyte imbalances, specifically potassium. Hypovolaemia
been described as systolic blood pressure greater than
and hypokalaemia are associated with haemodynamic
190 mmHg and/or diastolic greater than 100 mmHg.
instability during induction of anaesthesia and should
The initial approach should focus on identification
therefore be avoided. Patients taking diuretics who
and treatment of any underlying cause, for example,
present to pre-assessment should have their serum
providing appropriate analgesia. Once precipitants
electrolytes measured and advised to omit medication
have been addressed, subsequent measures should
on the day of surgery.
focus on a targeted approach to the pathophysiology
ACE inhibitors should also be discontinued the
of hypertension, for example, identifying increases
day before surgery. The renin-angiotensin-aldosterone
in the cardiac output or systemic vascular resistance
system is involved in maintenance of normotension
or both.
during anaesthesia. Inhibition is therefore associ-
Cardiac output may be raised in cases of good left
ated with refractory hypotension in the perioperative
ventricular function and in the presence of hypervol-
period and omission is recommended. Refractory
aemia and sympathetic activation. An associated tach-
hypotension may still occur with angiotensin II recep-
ycardia may be observed. In these instances, diuretics
tor blockers and they should be discontinued for
can be used to off-load the intravascular volume and
2 days prior to surgery.
beta-blockers to provide sympatholysis. Alternatively,
Hypertension is not uncommon in the anaes-
dihydropyridine calcium channel blockers or cen-
thetic room prior to induction. In most cases there
trally acting alpha-agonists such as clonidine can be
is a significant contribution from patient anxiety and
used with less negative inotropic effects. If hyperten-
reference should be made to the patient’s preopera-
sion is driven by raised vascular tone, a vasodilating
tive blood pressure as assessed at admission. During
agent would be an appropriate treatment. In circum-
induction for cardiac surgery, efforts are made to
stances where vascular tone has been chronically high,
avoid a dramatic reduction in arterial pressure whilst
replacement of the intravascular volume may also be
also preventing the pressor response associated with
required with vasodilation.
laryngoscopy. Traditionally, this has led to the use
of induction agent dose-sparing approaches such as
the use of high dose opiates and local anaesthetics. Specific Medications used in the
Intraoperatively, anaesthesia can be maintained by a
total intravenous or volatile approach. Volatiles, spe-
Management of Acute and Chronic
cifically isoflurane and to a lesser extent sevoflurane, Hypertension
have the additional advantage of being associated with There are several agents available for the management
myocardial preconditioning. Additionally, during of chronic hypertension. However, it is more chal-
stimulating periods such as sternotomy, volatiles can lenging to achieve an effective and sustained control
be used to rapidly deepen anaesthesia whilst also pre- of blood pressure in the acute care setting. In fact, if
venting the associated hypertensive response. Other many anti-hypertensive agents effectively lower blood
agents used specifically for their hypotensive effects pressure, only few have the capacity to achieve strict
include boluses of intravenous magnesium sulphate control of hypertension in the acute setting.
and fast acting beta-blockers such as esmolol. Ideally, The most commonly used anti- hypertensive
the blood pressure should be kept within 20% of the agents, with their advantages and disadvantages, are
baseline blood pressure. outlined in Table 30.4.
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268
Table 30.4 Commonly used anti-hypertensive agents
Class Drug name Mechanism of action Indications Contraindications Significant side

effects
Beta-blockers Labetalol Mixed alpha-and beta-AR Acute hypertension Asthma Hypotension
antagonist Pregnancy Acute heart failure Heart block
Maintaining cerebral perfusion Peripheral vascular disease Bronchospasm
Rate control in SVTs
Esmolol Selective beta-1-AR Acute hypertension Acute heart failure
antagonist Aortic dissection
Pregnancy
Alpha-blockers Phentolamine Non-selective alpha-AR Acute hypertension Pulmonary hypertension Orthostatic
antagonist Phaeochromocytoma hypotension
Cocaine intoxication Headache
.033
Urapidil Selective alpha1-AR Acute hypertension Aortic stenosis Tachycardia
antagonist Major AV shunt
Alpha2-blockers Clonidine Central alpha2-AR agonist Acute hypertension AV node disease Drowsiness
Sedation weaning Sinoatrial node disease Dizziness
Analgesia Headache
Fever
14:51:03
Dexmedetomidine Acute hypertension No absolute contraindication Hypotension
Sedation weaning Vomiting
Fever
Methyldopa Acute hypertension Active hepatic disease Drowsiness
Pregnancy Depression Headache
Muscle pain
Arterial vasodilators Hydralazine Direct arteriolar vasodilator Essential hypertension Aortic or mitral stenosis Headache
Hypertensive crisis Pulmonary hypertension Tachycardia
Congestive heart failure Lupus Muscle pain
Fenoldopam Selective dopamine receptor Hypertensive crisis Glaucoma Headache
1 agonist Severe hypertension Concomitant use of Nausea
beta-blocker Flushing
Calcium channel Nicardipine L-type calcium channel Short-term treatment of Aortic stenosis Headache
blockers blocker hypertension Flushing
(dihydropyridines) Muscle pain
Diltiazem L-type calcium channel Chronic hypertension Sick sinus syndrome Headache
blocker Chronic stable angina AV block Flushing
(non-dihydropyridines) Acute MI Muscle pain
Cough
Nitrites and nitrates Nitroprusside Nitric oxide donor Hypertensive crisis Vitamin B12 deficiency Headache
Active hepatic disease Flushing
Reduced platelet
aggregation
Ileus
Metabolic acidosis
ISMN Stable angina Acute heart failure Headache
Aortic/mitral stenosis Nausea
Dizziness
.033
Diuretics Furosemide Inhibition of Na/Cl/K Congestive heart failure Anuria Hearing loss
cotransporter Cirrhosis Itching
Renal disease Jaundice
Nausea
Vomiting
Bumetanide Inhibition of Na/Cl/K Congestive heart failure Anuria Nausea
cotransporter Cirrhosis Vomiting
14:51:03
Renal disease Itching
Dizziness
270
Special Circumstances • Reintroduction of preoperative anti-hypertensive

medication postoperatively should be
Hypertensive Crises cautiously considered in the context of the
cardiothoracic unit.
Severe or stage 3 hypertension associated with end-
organ damage is a medical emergency and patients
should be closely monitored with invasive monitor-
ing and managed in a high dependency area. Ideally
Further Reading
diastolic pressure should be reduced by no more than Chobanian AV. The Seventh Report of the Joint National
10–15% or less than 110 mmHg within an hour. More Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure: the JNC 7 report.
dramatic reductions may result in hypoperfusion due Journal of the American Medical Association. 2003;
to altered autoregulation of organ blood. This reduc- 289: 2560–2572.
tion typically requires the use of a short-acting intra-
Devereaux PJ, Yang H, Guyatt GH. Rationale, design, and
venous agent by continuous infusion. In the absence organization of Perioperative Ischemic Evaluation
of end-organ damage there is less urgency and blood (POISE) trial: a randomised controlled trial of
pressure can be lowered over a period of 1–2 days. metoprolol versus placebo in patients undergoing
noncardiac surgery. American Heart Journal. 2006;
Aortic Dissection 152: 223–230.
Gal TJ, Cooperman LH. Hypertension in the immediate
Aortic dissection itself is considered a hypertensive cri-
post-operative period. British Journal of Anaesthesia.
sis due to the associated end-organ damage. Pressure 1975; 47: 70–74.
related damage to the aortic intima results in a tear and
Lewington S, Clakre R, Qizilbash N, Peto R, Collins
passage of blood into the potential space between the R. Prospective Studies Collaboration: age-specific
intimal and medial layer. High arterial pressure pro- relevance of usual blood pressure to vascular
motes passage of blood into the false lumen and exten- mortality: a meta-analysis of individual data for one
sion of tear both distally and proximally. Under these million adults in 61 prospective studies. Lancet. 2002;
circumstances, aggressive blood control is required 361: 106Q.
and ideally should be achieved within minutes. Whilst National Institute for Health and Care Excellence.
such patients are likely to be chronic hypertensives and Guideline CG127. Hypertension: Clinical Management
therefore at risk of hypoperfusion and ischaemia, the of Hypertension in Adults. August 2011.
benefits of preventing or avoiding further dissection of Rajgopal R, Rajan S, Paul J. Effect of pre-operative
the aorta outweigh these risks. discontinuation of angiotensin-converting enzyme
inhibitors or angiotensin II receptor antagonists on
intra-operative arterial pressures after induction of
Key Points anaesthesia. Anethesia, Essays and Researches. 2014;
• The aetiology of hypertension in the 8: 32–35.
cardiothoracic critical care unit is often Stevens RD, Burri H, Tramer MR. Pharmacologic
multifactorial and may resolve with management myocardial protection in patients undergoing
of the underlying precipitant alone. non-cardiac surgery: a quantitative systemic review.
• Patients on established therapy, except for ACE Anesthesia & Analgesia. 2003; 97: 623–633.
inhibitors, should continue up until the day of Valchanov K, Arrowsmith JE. Do venodilators have
surgery unless specifically contraindicated. a role in the perioperative management of heart
failure? European Journal of Anesthesia. 2012;
• The initial approach of postoperative
29: 121–128.
management should focus on identification and
treatment of any possible underlying cause, for Vuylsteke A, Vincent JL, de la Payen GD, et al.
Characteristics, practise patterns and outcomes
example, providing appropriate analgesia. in patients with acute hypertension: European
• It is challenging to achieve an effective and registry for Studying the Treatment of Acute
sustained control of blood pressure in the acute Hypertension (Euro-STAT). Critical Care. 2011;
care setting. 15: R271.
14:51:03
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MCQs
1. Which of the following statements regarding hyper- (b) A blood pressure of 135/95 would be
tension are true? considered normal
(a) Blood pressure or mean arterial pressure (MAP) is (c) Hypertension seen in renal disease is classified as
considered the product of the stroke volume (SV) primary hypertension
and systemic vascular resistance (SVR) (d) Acute severe elevations in blood pressure are often
(b) Blood pressure or mean arterial pressure (MAP) is caused by the presence of end-organ damage
considered the product of the cardiac output (CO) (e) Secondary hypertension is less common in the
and systemic vascular resistance (SVR) and can be younger population
summarised as
4. Which of the following statements regarding hyper-
MAP (mmHg) = (HR × SV) × SVR tension management are true?
(c) Blood pressure or mean arterial pressure (MAP) is (a) Poorly managed or undiagnosed hypertension
considered the product of the heart rate (HR) and should be identified at surgical pre-assessment and
stroke volume (SV) appropriate treatment instigated in the immediate
(d) Hypertension can occur acutely only with an postoperative period
increase in systemic vascular resistance (SVR) (b) Presently beta-blockers are never recommended as
(e) Blood pressure or mean arterial pressure (MAP) is initial therapy for hypertension
considered the product of the cardiac output (CO) (c) Current practice advocates the discontinuation of
and heart rate (HR) both beta-blockers and calcium channel blockers
2. Which of the following statements regarding hyper- on the day of surgery
tension are true? (d) ACE inhibitors should be continued the day before
(a) In chronic primary or essential hypertension, surgery
decreases in vascular resistance and endothelial cell (e) Patients taking diuretics should be advised to omit
dysfunction result in sustained elevations in blood medication on the day of surgery
pressure
5. Which of the following statements regarding periop-
(b) Acute changes or swings in mean arterial pressure erative management of hypertension are true?
are sensed by baroreceptors found in the carotid
(a) At the time of surgery, ideally, the blood pressure
sinus and aortic arch. An increase in blood pressure
should be kept within 20% of the baseline blood
results in activation of a positive feedback reflex
pressure
loop whereby both heart rate and systemic vascular
resistance increase (b) Both hypervolaemia and hypokalaemia are
associated with haemodynamic instability during
(c) Autoregulation protects from the deleterious
induction of anaesthesia and should therefore be
effects of acute hypoperfusion or hyperperfusion.
avoided
However this only occurs within a range of mean
arterial pressures typically of 60–110 mmHg (c) Use of vasodilating agents is generally avoided in
postoperative patients
(d) In chronic hypertension, baroreceptors reset over
time to a lower level of mean arterial pressure (d) In case of hypertensive crisis, in the absence
of end-organ damage there is less urgency and
(e) In chronic hypertension, the autoregulation curve is
blood pressure can be lowered over a period of
shifted to the left for a given mean arterial pressure
1–2 days
3. Which of the following statements regarding hyper-
(e) Calcium channel blockers or centrally acting alpha-
tension are true?
agonists such as clonidine cannot be used because
(a) Grade 2 hypertension is characterised by a diastolic of their negative inotropic effects
pressure of 100–109 mmHg and a systolic pressure
of 160–170 mmHg
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272
Pulmonary Hypertension in the

Chapter

Mark Toshner and Joanna Pepke-Zaba
Introduction causes of transient PH in acutely ill patients. There

are therefore three distinct patient populations when
Pulmonary hypertension (PH) represents a group of
considering managing PH in the ITU: (1) those with
conditions which share the haemodynamic definition
recognised PH, (2) those with occult or unrecognised
of a mean pulmonary artery pressure equal or greater
PH and (3) those who develop PH as a consequence of
than 25 mmHg at rest. Acute pulmonary hyperten-
their acute illness. Compounding this challenge is the
sion in critical care may often be secondary to acute
paucity of evidence of how to manage any of these dif-
respiratory failure, left heart failure and pulmonary
fering groups and often the same evidence-free treat-
thromboembolism or due to decompensated chronic ment approaches are trialed regardless of aetiology.
pulmonary hypertension by concurrent comorbid Patients with PH most commonly die of right ven-
conditions. Pulmonary hypertension can complicate tricular (RV) failure and its consequences, regardless
perioperative management in patients admitted for of whether it is acute or chronic. Any rise in pulmo-
elective surgical procedures to treat their underlying nary vascular resistance (PVR) triggers RV dysfunc-
pulmonary hypertension (e.g. pulmonary endarterec- tion, and impaired RV adaptation to rapid increases in
tomy, lung transplantation). afterload results in ‘ventriculoarterial uncoupling’, RV
In the assessment of patients with PH, the pulmo- distension, myocardial oxygen consumption/delivery
nary capillary wedge pressure (PCWP) is of impor- imbalance and heart failure. It is important to recog-
tance in discriminating between pulmonary arterial nise that the right and left ventricles (LV) are not sep-
(precapillary) and venous hypertension (postcapil- arate organs and functionally impact on each other.
lary). Current guidelines use the cut-off of 15 mmHg Not only do they share an interventricular septum,
to differentiate but it is important to acknowledge the but 25% of the cross-fibres in the RV are common to
preload dependent nature of the PCWP, which can the LV. Significant RV–LV interdependence exists in
be affected in particular by fluid status. Pulmonary the setting of RV pressure and/or volume overload,
hypertension is commonly thought of as a rare dis- reduced RV stroke volume, reduced LV venous return
ease but in reality is commonly associated with var- leading to impaired LV filling contributing to the fall
ied pathophysiological processes. This is reflected in in cardiac output and heart failure. In acute causes
current classification systems, which highlight just of PH the RV is unprepared to cope with a resultant
how many diseases can result in PH. Evidence from inability to generate very high pressures and there is
primary care suggests that up to 13% of all-comers an easily breached contractile reserve. In chronic PH
to open access breathlessness clinics may have echo- the RV ability to ‘cope’ will partly rely on its coupling
cardiographic evidence of PH, and many of these to the pulmonary circuit. This will be dependent on
patients remain essentially undiagnosed either due to the degree of disease but also varies between disease
lack of awareness of the managing physicians or fatal- processes. More explicitly, how the RV copes is not
istic attitudes about prognosis. A particular problem linearly linked to simple pressure and resistance. This
lies in the classification categories where treatment was elegantly demonstrated in a mechanical animal
with targeting PH therapies has not been of proven model of chronic progressive RV pressure overload
benefit, especially groups 2 and 3, pulmonary venous (pulmonary artery banding). Despite identical pres-
hypertension and hypoxic lung disease. Additionally sure profiles to an established model of angioprolif-
the current classification system does not consider erative pulmonary hypertension (sugen/hypoxia), the
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Chapter 31: Pulmonary Hypertension
banding model does not develop RV failure but the whilst trying to offload. Control of pulmonary artery
sugen/hypoxia does. This is borne out clinically most pressure could be improved by treatment with high
notably in congenital heart disease where suprasys- flow oxygen as a selective pulmonary vasodilator in
temic pressures can develop but long-term outcomes patients with pulmonary hypertension, regardless of
are generally better than for other forms of PH. Added the underlying diagnosis, baseline oxygenation or
to this is the recognition that although pulmonary RV function. Anticoagulation may be desirable due
arterial hypertension (PAH) traditionally is thought to the low cardiac output states usually seen, and
of as affecting the small precapillary vessels, there should be considered. There is however no evidence
is heterogeneity of vascular compartments affected basis for this. Mechanical ventilatory support may be
across the spectrum of causes of PH (involving both considered depending on the underlying pathology,
precapillary and postcapillary compartments). This in particular if there is an identifiable and reversible
heterogeneity may in part explain the difficulty trans- cause of the PH. If the patient is a potential transplant
lating the success of treating PAH with pulmonary candidate this should be considered. ECMO is largely
vasodilators to most of the other causes. Therefore all currently restricted to bridging patients to transplan-
‘PH’ is not the same from a biomechanical or treat- tation; however its role may evolve.
ment response perspective.
In this chapter we will clarify what evidence-based Treatment of Underlying Causes
medicine and expert consensus is available and the The underlying disease process should be improved or
impact on management and treatment strategies in optimised. For example, with left heart failure, ther-
the intensive care unit (ICU). Explicitly we will dis- apy needs to be optimised, ventilation in lung dis-
cuss managing the patient with known PH, and how eases needs to be optimised and antibiotics used if an
to approach patient populations at risk. infective process is suspected. Specific attention should
be paid to avoiding respiratory acidosis and meta-
bolic acidosis. This can be limited by maximisation of
Supportive Care and General recruitment of lung alveoli and optimisation of venti-
Management of PH in the ICU lation-perfusion matching by patient positioning and
Acutely unwell patients need to be moved to a criti- optimisation of ventilation and positive end expiratory
cal care environment. Appropriate investigations and pressure. All attempts should be made to reduce PVR
monitoring should aim to identify and reverse precip- in PAH patients presenting with heart failure. An excel-
itating factors, especially those associated with a high lent example of successful management of patients in
mortality. the ICU with significant pulmonary hypertension is
Optimal fluid balance is paramount, as both hypo- chronic thromboembolic pulmonary hypertension
volaemia and hypervolaemia may be detrimental to (CTEPH) patients treated with pulmonary endarterec-
cardiac output. In hypervolaemic patients, reducing tomy (PEA). This represents the largest cohort of PH
RV preload through diuresis will improve RV func- patients successfully managed in the ICU. Mortality
tion, RV-LV interdependence and LV diastolic compli- rates in high-volume centres are now down as low as
ance. Patients with decompensated RV failure develop 2–5%. Despite this, these patients are often not consid-
secondary hyperaldosteronism and addition of an ered when assessing the evidence on how to manage
aldosterone antagonist, such as spironolactone, to a patients with established PH. This is understandable as
loop diuretic can be useful. In the critically ill patient the majority of patients have significant early reduction
with PH and right heart failure it is a constant and in pulmonary pressure and resistance, and therefore are
delicate balancing act getting the fluid balance right. not comparable from this perspective to other groups
The most common mistake is overfilling patients who of PH patients. The clearest lesson from PEA is that
are already fluid overloaded in an attempt to bolster patients with PH can be successfully managed in the
systemic blood pressure. In the context of right heart ICU but most notably when the cause of the increased
failure it is likely that patients will be overfilled and resistance is treatable. In patients where the cause of
therefore maintaining a negative balance is critical in the PH is unknown or unclear, consideration should be
the majority of cases. Underfilling, however, will affect given to rarer causes of PH and investigations tailored
LV output and systemic blood pressure. We are there- to identify potentially reversible causes. The current
fore often left in a situation considering vasopressors classification of PH aetiology is delineated in Table 31.1.
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Table 31.1 NICE classification of pulmonary hypertension

To Monitor or Not To Monitor?
1. Pulmonary arterial hypertension The standard assessment of non-invasive haemody-
1 Idiopathic namic and renal, hepatic and neurological function will
1.2 Heritable provide direct and surrogate information on cardiac
1.2.1 BMPR2 mutation
status, but beyond this there is no good evidence for
1.2.2 ALK-1, ENG, SMAD9, CAV1, KCNK3
1.2.3 Unknown
or against additional monitoring. Echocardiography
1.3 Drugs and toxins induced will potentially be diagnostically useful and can give
1.4 Associated with: extra information such as the presence of pericardial
1.4.1 Connective tissue disease effusions but has no clear role in monitoring. This is
1.4.2 HIV infection largely due to the complicated physical nature of the
1.4.3 Portal hypertension RV, which makes bedside echo assessment of function
1.4.4 Congenital heart disease
crude at best. Invasive cardiac monitoring is no longer
1.4.5 Schistosomiasis
in vogue in the ICU having proven of no benefit in
1ʹ Pulmonary veno-occlusive disease and/or pulmonary capillary
haemangiomatosis
the management of critically ill general ICU patients
1ʺ Persistent pulmonary hypertension of the newborn
or in high-risk postoperative cohorts. There is a lack
of trials looking specifically at PH and therefore any
2. Pulmonary hypertension due to left heart disease
advice is based on theory and opinion. However, most
2.1 Left ventricular systolic dysfunction
expert reviews still recommend invasive monitoring
2.2 Left ventricular diastolic dysfunction
2.3 Valvular disease
by pulmonary artery catheter (PAC) of PA pressure,
2.4 Congenital/acquired left heart inflow/outflow tract cardiac output and PCWP, though not unambigu-
obstruction and congenital cardiomyopathies ously. There are non-invasive methods for measuring
2.5 Congenital /acquired pulmonary veins stenosis cardiac output on its own, such as bioimpedance, bio-
3. Pulmonary hypertension due to lung diseases and/or reactance and pulse wave analysis, though again there
hypoxia are no data strongly supporting a role in guiding treat-
3.1 Chronic obstructive pulmonary disease ment decisions. Monitoring and basic investigations
3.2 Interstitial lung disease are outlined in Table 31.2.
3.3 Other pulmonary diseases with mixed restrictive and
obstructive pattern
3.4 Sleep disordered breathing Resuscitation In and Outside
3.5 Alveolar hypoventilation disorders
3.6 Chronic exposure to high altitude
of the ICU
3.7 Developmental lung diseases
Patients with PH have been demonstrated to have very
poor outcomes in a large but retrospective analysis
4. Chronic thromboembolic pulmonary hypertension and
other pulmonary artery obstructions of tertiary care centres. This included all comers but
4.1 Chronic thromboembolic pulmonary hypertension
reflected the nature of specialist centres with 49% of
4.2 Other pulmonary artery obstructions
4.2.1 Angiosarcoma Table 31.2 Monitoring and investigations for pulmonary
4.2.2 Other intravascular tumours hypertensive patients
4.2.3 Arteritis
4.2.4 Congenital pulmonary artery stenois Monitoring Investigations
4.2.5 Parasites (hydatidosis) Weight and fluid balance WCC/CRP/blood and urine
5. Pulmonary hypertension with unclear and/or cultures
multifactorial mechanisms BP/pulse ± non-invasive CO CXR
5.1 Haematological disorders: chronic haemolytic anaemia, O2 sats and ABGs Troponin
myeloproliferative disorders, splenectomy
5.2 Systemic disorders, sarcoidosis, pulmonary histiocytosis, Lactate HRCT PA
lymphangioleiomyomatosis Invasive haemodynamics Right ventricular assessment
5.3 Metabolic disorders: glycogen storage disease, Gaucher • CVP • 12-lead ECG and continuous
disease, thyroid disorders • MPAP monitoring
5.4 Others: pulmonary tumour thrombotic microangiopathy, • PACWP • Echocardiography
fibrosing mediastinitis, chronic renal failure (with/without • NT-proBNP
• CO/mixed venous O2
dialysis), segmental pulmonary hypertension
• Non-invasive CO
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the patients reported having a diagnosis of idiopathic

PAH and the majority of the rest being either group 1
Catecholamines
In a study of 27 patients undergoing surgery for left-
PAH or CTEPH. Only eight patients (6% of the sur-
sided valvular replacement and congenital heart dis-
vey) survived to 90 days without significant neurologi-
ease, there were increases in systemic pressure and
cal damage. This was despite the very high proportion
pulmonary artery pressure with both phenylephrine
of 63% of the patients already being located in the ICU.
and noradrenaline. Nineteen of the 27 patients were
Of these patients, all but one had an identifiable revers-
postcapillary PH with mitral valve replacement (MVR).
ible cause for their arrest such as vasovagal reactions,
Of interest there were no significant changes in cardiac
digitalis toxicity or pericardial tamponade. The mean
output and surprisingly heart rate did not change.
pulmonary vascular resistance in this cohort was very
There are conflicting data on the effects of dopa-
high at 1694 dyne s/cm5 and it is probably extremely
mine, possibly attributable to the mixed populations
difficult to achieve effective pulmonary blood flow
studied. Initial studies in stable patients and healthy
and left ventricular filling with chest compressions in
controls suggested heart rate, mPAP, aortic mean pres-
this context. Therefore in the ICU it is appropriate in
sure and CI increased, while SVR reduced. PVR did not
all PH patients, and specifically those with PAH, to
change significantly. In studies in over 1600 patients
address early the plans for escalation in the event of an
in the ICU (not however stratified by PH), dopamine
arrest, with a clear understanding that in the absence
caused an excess of arrhythmias when compared with
of reversible causes, success is unlikely.
noradrenaline and in subanalyses of patients with car-
diogenic shock, an excess of deaths. When using dopa-
Acute Medical Therapy mine in PH patients, who are prone to arrhythmias,
physicians should be particularly alert to this possibility.
Vasopressors in PH
It is facile to state the importance of maintaining Vasopressin
systemic blood pressure in the context of critically In a case series of nine valve replacement patients
unwell populations, however in PH there is the addi- who presented with postoperative refractory vasodi-
tional challenge of making sure systemic pressure latory hypotension concomitant with PH, vasopressin
exceeds PA pressure and therefore maintaining right increased mean systemic arterial pressure but at the
coronary artery perfusion. The right coronary perfu- expense of reduced cardiac output. Changes in PVR
sion cycle differs from the left in that it occurs more did not reach significance.
diffusely and peaks in systole. To do this using vaso-
pressors presents a number of challenges. The first is Dobutamine
the inability to selectively spare the pulmonary circu- In nine cirrhotic patients with mild PH undergoing
lation from the vasopressor effect. The second is the liver transplantation, there was an increase in RV con-
effect on heart rate and rhythm, cardiac function and tractility and decrease in afterload when dobutamine
output. was infused in the anhepatic phase. Mean pulmonary
Animal studies are limited. In an experimental arterial pressure (mPAP) went up by 4 mmHg and car-
dog model of acute RV failure by pulmonary artery diac index (CI) doubled from 2.3 to 5.1 l/min/m2 with
constriction, the administration of phenylephrine an overall reduction in pulmonary vascular resist-
decreasing RV afterload, increasing aortic pressure ance (PVR). In acute studies in patients with mixed
and hence myocardial perfusion pressure increases lung diseases being assessed for lung transplantation,
myocardial blood flow, reverses ischaemia and dobutamine also increased CI and mPAP (though not
improves RV function. Despite this potentially posi- statistically significant). Again this appeared to result
tive effect of vasopressors on RV function, in human in an overall reduction in PVR, suggesting that there
studies the effects are more complex and potentially may be some recruitment of vessels given the absence
antagonistic. There are effectively no high quality large of any reduction in pressure.
randomised controlled data for vasopressors and ino-
tropes in PH ICU patients. Care therefore needs to be Levosimendan
taken in interpreting the available data and also note Levosimendan sensitises calcium and acts as a vaso-
made of the heterogeneity of the studied populations. dilator in addition to putative inotropic effects, which
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have been suggested to be of potential benefit. The Endothelin receptor antagonists are not often consid-
evidence for levisomendan is however weak. A small ered as it takes time to establish their action.
placebo randomised clinical trial (RCT) in 28 patients
with mixed aetiology PH was undertaken using levo- Conclusions
simendan. This was in stable patients, not in the ICU, Pulmonary hypertension is complicated and difficult to
and administered using short-term infusions 4 times at manage in the ICU. Usually it is complicated by right
2-week intervals. There were only significant changes ventricular failure. The first question that should be
in PVR demonstrable acutely at 24 hours and not at asked is related to the aetiology of pulmonary hyperten-
8 weeks, and surprisingly there was 25% deterioration sion – Is this pre-existing PH, occult PH or PH associated
in the PVR in the placebo group, which is difficult to with the acute illness? As is often the case, identifying the
explain. Hypotension was a significant side effect. cause will dictate treatment. Medical management relies
on the attention to volume status and contractile state of
the right ventricle and requires complex decision mak-
Pulmonary Vasodilators ing on risk/benefit considerations in the absence of a
We will not attempt to summarise the literature on definitively correct evidence-based approach. There is a
pulmonary vasodilators in PH but restrict ourselves need for well-controlled and well-designed prospective
to the limited data and expert opinion on their use in research in PH in the ICU to clarify best practice.
ICU populations. Inhaled NO has been most widely
used because of its selective action on the pulmonary
circulation. The occurrence of rebound pulmonary
Learning Points
• Patients with pulmonary hypertension present
hypertension when administration is interrupted has
with right ventricle failure due to different disease
limited its use. The inhaled prostacyclin analogue
states. Determining the underlying aetiology can
iloprost is a valuable alternative, inducing more pro-
be critical to treatment.
nounced haemodynamic improvement acutely. The
only randomised blind trial of nitric oxide in PH • Management should concentrate on maximal
was in cardiopulmonary bypass patients undergoing reduction of RV afterload based on underlying
mitral valve surgery with a PVR of over 200 dynes pathophysiology including adequate coupling of
s/cm5. This trial of inhaled NO at 20 ppm enrolled 58 RV contractility to vascular load.
patients but was a comparator trial to nitroprusside • Haemodynamic monitoring can be essential
and inhaled prostacyclin. Prostacyclin and NO both to provide adequate data on which to base
reduced mPAP and consequently PVR (by 50 and management decisions.
45% respectively) but with no significant effect on • Optimal fluid balance is paramount.
other haemodynamic parameters. The converse was • There is a paucity of evidence for the therapies
also seen in a small and uncontrolled trial in seven used for LV failure and PAH for management of
patients with PH post left ventricular assisted device pulmonary hypertension and right ventricular
(LVAD) insertion where withdrawal of NO resulted in failure in the ICU settings.
a significant increase in PVR. Post cardiac transplan-
tation, both NO and prostacyclin decrease PVR with Further Reading
no change in SVR with NO but a decrease in SVR with Bogaard HJ, Natarajan R, Henderson SC, et al. Chronic
prostacyclin administered intravenously. Thirteen pulmonary artery pressure elevation is insufficient
patients post inferior myocardial infarct with cardio- to explain right heart failure. Circulation. 2009;
genic shock behaved broadly the same in an uncon- 120: 1951–1960.
trolled study with an additional increase in CI of 24%. Cannon JE, Su L, Kiely DG, Page K. Dynamic risk
There is a cost implication as NO is considerably more stratification of patient long-term outcome after
expensive. In 18 consecutive heart transplant patients, pulmonary endarterectomy: results from the
9 with PH, there was a modest 5 mmHg drop in mPAP United Kingdom national cohort. Circulation. 2016;
with nebulised milnirone. Sildenafil (oral or intrave- 133: 1761–1771.
nous) has no good quality data in the ICU setting but is De Backer D, Biston P, Devriendt J, et al. Comparison of
often considered largely because of the reasonable side dopamine and norepinephrine in the treatment of shock.
New England Journal of Medicine. 2010; 362: 779–789.
effect profile. It can still cause systemic vasodilatation.
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Fattouch K, Sbraga F, Bianco G. Inhaled prostacyclin, nitric Hoeper MM, Granton J. Intensive care unit management
oxide, and nitroprusside in pulmonary hypertension of patients with severe pulmonary hypertension and
after mitral valve replacement. Journal of Cardiac right heart failure. American Journal of Respiratory and
Surgery. 2005; 20: 171–176. Critical Care Medicine. 2011; 184: 1114–1124.
Friedberg MK, Redington AN. Right versus left ventricular Hoeper MM, Olschewski H, et al A comparison of the
failure: differences, similarities, and interactions. acute hemodynamic effects of inhaled nitric oxide
Circulation. 2014; 129: 1033–1044. and aerosolized iloprost in primary pulmonary
Galie N, Humbert M, Vachiery JL. 2015 ESC/ERS hypertension. German PPH study group. Journal of the
Guidelines for the diagnosis and treatment of American College of Cardiology. 2000; 35: 176–182.
pulmonary hypertension: The Joint Task Force for the Hoffman D, Sisto D, Frater RW. Left-to-right ventricular
Diagnosis and Treatment of Pulmonary Hypertension interaction with a noncontracting right ventricle.
of the European Society of Cardiology (ESC) and Journal of Thoracic and Cardiovascular Surgery. 1994;
the European Respiratory Society (ERS): Endorsed 107: 1496–1502.
by: Association for European Paediatric and Kwak YL, Lee CS, Park YH. The effect of phenylephrine
Congenital Cardiology (AEPC), International Society and norepinephrine in patients with chronic
for Heart and Lung Transplantation (ISHLT). European pulmonary hypertension. Anaesthesia. 2002; 57: 9–14.
Heart Journal. 2016; 37: 67–119.
Sandham JD, Hull RD, Brant RF. A randomized, controlled
Gaynor SL, Maniar HS, Bloch JB. Right atrial and trial of the use of pulmonary-artery catheters in high-
ventricular adaptation to chronic right ventricular risk surgical patients. New England Journal of Medicine.
pressure overload. Circulation. 2005; 112: I212–I218. 2003; 348: 5–14.
Harvey S, Harrison DA, Singer M. Assessment of the Sibbald WJ, et al. Pulmonary hypertension in
clinical effectiveness of pulmonary artery catheters sepsis: measurement by the pulmonary arterial
in management of patients in intensive care (PAC- diastolic-pulmonary wedge pressure gradient and the
Man): a randomised controlled trial. Lancet. 2005; influence of passive and active factors. Chest. 1978;
366: 472–477. 73: 583–591.
MCQs
1. Best general medical supportive care of PH patients (d) Pulmonary vasodilators
on ICU includes: (e) All of the above
(a) Oxygen therapy
4. The best way of monitoring pulmonary arterial pres-
(b) Optimisation of fluid balance sure is by using:
(c) Anticoagulation (a) Central venous pressure
(d) ECMO (b) Mean PAP
(e) All except ECMO (c) Pulmonary capillary wedge pressure
2. Appropriate volume management may involve: (d) Cardiac output/mixed venous O2
(a) Intravenous loop diuretics (bolus, continuous (e) Arterial blood gases
infusion)
5. The most commonly used pulmonary vasodilator
(b) Addition of thiazide diuretic which avoids significant systemic vascular side effects
(c) Maintenance of a negative fluid balance in PH patients on the ICU is:
(d) Addition of inotropes if low cardiac output (a) NO
(e) All of the above (b) Prostacyclin
3. Treatment of underlying causes of PH involves: (c) Phosphodiesterase 5 inhibitors
(a) Steroids if coexisting asthma suspected (d) Endothelin receptor antagonist
(b) Optimisation of gas exchange in lung diseases (e) GTN
(c) Antibiotics if an infective process is suspected
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The Infected Patient

Chapter
32 Simon J Finney
Infection is a common problem for patients in cardio- Clinicians often use laboratory investigations
thoracic intensive care units (CT ICUs) and although to guide their assessment of the presence of infec-
it may be the primary reason for admission, many tion. However, it is normal for the C-reactive pro-
more infections are acquired on the ICU. Estimates of tein (CRP) and white cell count to increase following
incidence rates vary but are at least 5%. Undoubtedly, cardiac surgery even in the absence of infection;
infection increases morbidity, the length of ICU whether the magnitudes of these changes are greater
admission and mortality. in the setting of concomitant infection is not clear.
This chapter considers infected patients in general Procalcitonin (PCT) is a peptide biomarker that has
along with specific infections of particular impor- greater sensitivity and specificity for bacterial sepsis,
tance to patients admitted to the cardiothoracic ICU. and its resolution, than other cytokines or CRP. It
Antibiotic therapy is considered in Chapter 12. Patients has been employed in general populations of criti-
undergoing thoracic transplantation (Chapter 40 and cally ill patients to limit the initiation or duration of
Chapter 41) are particularly prone to infections and antibiotic therapy. PCT rises following cardiopulmo-
susceptible to a wider range of pathogens. nary bypass with levels exceeding thresholds used in
other populations to define bacterial infection. Even
Identification of Infected Patients higher levels of PCT are observed with infection fol-
Many patients develop systemic inflammation following cardiac surgery, but whether modifying anti-
lowing major surgery and cardiopulmonary bypass. It microbial practices based on these higher thresholds
can be difficult to distinguish those in whom infec- impacts on patient outcomes has never been tested.
tion is the aetiology from the signs and symptoms of Moreover, in one study over half of patients with
inflammation. mediastinal infections did not have increased PCT
The identification of patients with sepsis and sep- levels.
tic shock used to be based on heart rate, tempera- The nature of the infecting organisms may be
ture, respiratory rate and the leucocyte count in the revealed by standard microbiological investigations of
context of suspected infection. These criteria have samples from normally sterile sites. Frequently these
poor predictive value of organ dysfunction and out- investigations are negative in the context of prior ini-
come in patients following cardiac surgery, maybe tiation of antibiotic therapy. Molecular techniques
in part because they can be modified by recent car- such as 16S RNA sequencing of tissues and fluids can
diopulmonary bypass or concomitant therapies such be invaluable in settings such as infective endocar-
as mechanical ventilation, pacing and renal replace- ditis where standard techniques fail due to the pres-
ment therapy. Recently, the consensus definition of ence of antibiotics or fastidious organisms. Similarly,
sepsis has been modified and examines changes in PCR based assays of respiratory samples can identify
the sequential organ failure score (SOFA) from base- pathogenic viruses and Pneumocystis jirovecii rapidly.
line (see Table 32.1). This new system has not been 1,3 beta-D-glucan assay, mannan and anti-mannan
validated specifically in the cardiothoracic patient but antibody assays may help diagnose invasive fungal
may be more useful. However, since organ dysfunc- infection. Close liaison with a clinical microbiologist
tion can be the result of an inadequate cardiac output, or infectious disease specialist is important.
patients may have elevations in their SOFA score for Therefore, ultimately the diagnosis of an infected
an alternative reason. patient is based on clinical judgement of the clinical
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Chapter 32: The Infected Patient
Table 32.1 SOFA (sequential organ failure assessment) score
Variables 0 1 2 3 4
Respiratory >400 <400 <300 <200 <100
PaO2/FiO2 mmHg
Coagulation >150 <150 <100 <50 <20
Platelets × 103/μl
Cardiovascular No hypotension MAP Dopamine Dopamine >5 μg/kg/min Dopamine >15 μg/kg/min
Hypotension <70 mmHg <5 μg/kg/min Epinephrine <0.1 μg/kg/ Epinephrine >0.1 μg/kg/min
min, or Norepinephrine >0.1 μg/
Norepinephrine <0.1 μg/ kg/min
kg/min
Central 15 13–14 10–12 6–9 <6
nervous system
Glasgow coma
scale
Renal <1.2 1.2–1.9 2.0–3.4 3.5–4.9 >5.0 or <200
Creatinine μg/dl
OR
Urine output ml/dl
Liver <1.2 1.2–1.9 2.0–5.9 6.0–11.9 >12
Bilirubin mg/dl
setting, laboratory results cogniscent that they may The hallmark circulatory changes associated with
change for other reasons, microbiological data severe infection are arterial and venous vasodilatation
available and other investigations such as the chest and increased vascular permeability resulting in tis-
radiograph. sue oedema. This causes systemic hypotension that
is mitigated normally by the physiological response
General Clinical Management of an increased cardiac output. Healthy adults can
The Surviving Sepsis Campaign has done much to edu- increase their cardiac index to well in excess of
cate clinicians about sepsis. It has created evidence- 4–5 l/min/m2. This may not be possible in those with
based guidelines for the management of patients heart failure, valvular heart disease or with therapies
with sepsis which are wide ranging and cover many such as beta-adrenoreceptor blockade. Typically, cli-
aspects of care including antibiotic therapy, processes nicians administer considerable volumes of intravas-
of care, management of concomitant respiratory fail- cular fluid to combat the increased venous compliance
ure and fluid resuscitation. Protocolisation of aspects and hypotension. However, consideration should be
of care has been associated with improved outcomes. given to the effects of further fluid administration on
Some of the key recommendations are highlighted in stroke volume (the primary goal of fluid administra-
Table 32.2 and these are equally applicable to patients tion) and the balance between the need to increase car-
with cardiothoracic illness. diac output versus the need to increase vascular tone
The guidelines published in 2012 have been modi- with drugs such as noradrenaline and vasopressin.
fied recently to remove specific goals of initial fluid Consideration of these factors is ever more important
resuscitation based on the central venous pressure in those with cardiac disease. For example, excessive
and venous oxygen saturations. Three well-conducted fluid administration may adversely affect right ven-
large multicentre randomised trials –ProMISe, tricular dysfunction, which may be exacerbated by
ProCess and ARISE –did not demonstrate a benefit of the increase in pulmonary vascular resistance that
targeting these parameters during initial fluid resusci- can occur during sepsis and systemic inflammation.
tation. Moreover, it is likely that optimal fluid resusci- Hypotension can be exacerbated further by the myo-
tation strategies may differ in patients with intrinsic cardial dysfunction related to systemic sepsis per se.
cardiac dysfunction. In some settings inotrope therapy may be indicated.
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Table 32.2 Excerpt from Surviving Sepsis (2012) recommendations
Recommendation Grade of recommendation*

Give antibiotics early 1B (septic shock)
1C (severe sepsis)
Identify (e.g. take microbiological cultures) and control the source of infection early, for 1C
example drain an abscess
Crystalloids are the first choice for intravascular fluid replacement 1B
Human albumin solution can be considered in patients requiring considerable amounts of 1C
crystalloid; avoid starch solutions
Noradrenaline is the first choice vasopressor 1B
Protocolised blood sugar management should aim for a blood glucose <180 mg/dl (10 mM) 1A
Hydrocortisone (200 mg/day) should only be considered if fluids and vasopressors do not 2C
restore haemodynamic stability
* Grade 1 recommendations are strong; Grade 2 are weak. The quality of the evidence is indicated as high (A, based on randomised
controlled trials), moderate (B, downgraded RCTs or upgraded observational studies), low (C, well conducted observational studies with
control RCTs) or very low (D, downgraded controlled studies or expert opinion).
No study demonstrates a specific inotrope to be supe- such as central lines or pacing systems. It is generally
rior, but anecdotally milrinone is often associated tolerated better haemodynamically than left sided dis-
with worsening vasoplegia and many prefer dobu- ease. Right sided endocarditis presents typically with
tamine or small to moderate doses of adrenaline. A multiple pulmonary septic emboli which may be man-
recent study of levosimendan, a myocardial calcium ifested by breathlessness, chest pain and haemoptysis.
sensitiser, showed no advantage in preventing organ Antimicrobial therapy is the cornerstone of ther-
dysfunction or mortality in sepsis. apy in IE and choice of antibiotic is influenced by
Corticosteroids have been demonstrated to whether the endocarditis is on a native valve or pros-
reduce the duration of hypotension in a general criti- thetic valve, the organism and the minimum inhibi-
cal care population whilst not impacting on mortal- tory concentration (MIC) for a particular organism/
ity. Restoration of the shock state may beneficially antibiotic combination. There is less emphasis on ami-
enhance coronary perfusion in those with coronary noglycosides in recent guidelines due to renal toxicity.
artery disease or significant right heart failure due to Rifampicin should not be instituted immediately as it
pulmonary hypertension. probably has an antagonistic effect against other anti-
biotics with respect to replicating bacteria.
Management of Specific Infections Heart failure may occur due to severe valvular
regurgitation, a fistula (e.g. an acquired Gerbode ven-
Endocarditis triculoatrial defect) or rarely valvular obstruction.
Infective endocarditis (IE) is a challenging condition Severe heart failure refractory to medical therapies is
with poor outcomes for patients. In hospital mortality an indication for expedited surgery.
rates are as high as 30%. Its incidence is increasing at Uncontrolled infection must be considered when
least in part due to the increasing number of patients fever persists or there is progressive perivalvular
at risk, for example those with intracardiac prosthetic extension of infection as manifest by complications
material. such as an aortic root abscess, fistula or pseudoaneu-
The management of infective endocarditis is com- rysms. Typically blood cultures become negative in a
plex and best undertaken by teams. Critical care phy- few days. New prolongation of the PR interval should
sicians are often involved either following valvular raise suspicion of aortic root abscesses.
interventions or if patients present with complications Cerebral embolisation from left sided endocardi-
such as heart failure, uncontrolled infection or embo- tis is a concern and can be associated with haemor-
lisation. Right sided endocarditis is less common and rhagic transformation too. The risks of embolisation
more often associated with intravenous drug abuse, fall progressively following institution of antimicro-
congenital heart disease or invasive vascular devices bial therapy.
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Surgery during the active phase of endocarditis pulmonary pathology are key factors underpinning
has high risks and in general it is deferred until 4–6 these increased risks.
weeks. Nevertheless it may be expedited in the setting Several interventions can lower the incidence of
of severe heart failure, uncontrolled infection or pre- VAP (see Table 32.3). They are often bundled together
vention of emboli. with other interventions that ventilated patients may
benefit from in a quality improvement strategy. Most
Infections of Implanted Devices aim to prevent contamination of the respiratory
tract by colonised oral secretions or reflux of gastric
Infection of implanted pacing systems or cardio-
contents.
verter defibrillators is increasing as more devices are
Caring for patients in a semi-recumbent position
inserted. It can be difficult to manage and may be
rather than supine reduces VAP rates. The optimal
associated with mortality as high as 10–22%. Infection
position is not known, but most aim for an angle of
can be in one or more of the endocardium, leads, or
over 30°.
device and its pocket. Estimates of the incidence range
Whilst peptic ulcer prophylaxis reduces the mor-
from 0.5% to 2.2%. Risk factors for infection include
bidity related to stress ulceration, it does so at the
inexperienced operators, low frequency of air changes
expense of increasing the incidence of VAP. Thus H2
in the operating environment, diabetes mellitus and
antagonists and proton pump inhibitors should be
renal failure. Management strategies include antibiot-
discontinued in those at low risk of stress ulceration
ics and device removal. Device removal may be com-
such as those that are fully fed enterally, do not have
plex in those who are dependent on a device and if
low cardiac output states, are not systemically anti-
leads have been present for some time when they may
coagulated and with no prior history of peptic ulcer
become adherent to vascular structures. Device and
disease.
lead removal may be complicated by bleeding, tam-
Studies of oral decontamination with chlorhex-
ponade, pulmonary embolism and death.
idine have had mixed results in the general criti-
Infection is a frequent complication of long term
cal care population. Two meta-analyses suggest that
durable ventricular assist devices. Driveline infec-
patients who have undergone cardiac surgery particu-
tion is the most common and usually occurs at the
larly benefit from this strategy. It has an unpleasant
exit site but infections may occur anywhere along the
taste for patients and does not obviate the use of fluo-
driveline up to the device pocket, or in the device or
ride containing toothpaste too.
cannulae. Typically there is local trauma at the exit
Daily interruptions or retitration of sedative medi-
site or an inadvertent tug on the line. This underpins
cations reduced the duration of mechanical ventila-
the careful initial surgical placement of the driveline
tion and thus the exposure of individual patients to
and dressings that stabilise the line. Management
the risk of acquiring a VAP. It may reduce the inci-
strategies include the simultaneous use of antibiotics,
dence of VAP per se.
fastidious exit site cleaning and source control with
The benefits of subglottic suctioning on endotra-
debridement of infected tissue and drainage of collec-
cheal tubes have been demonstrated in two meta-
tions. Rarely, device exchange or cardiac transplanta-
analyses. Suctioning reduces the pool of oral
tion may be considered.
sections that collect above the endotracheal cuff
and thus may reduce the contamination of the lower
Ventilator Associated Pneumonia respiratory tract. The cost of the endotracheal tubes
Ventilator associated pneumonia (VAP) is common may act as a barrier for their use in all cardiotho-
following cardiac surgery, with an estimated incidence racic surgical procedures, and the value of routine
of 21–27 cases per 1000 ventilator days. It is more changes in patients who stay over a defined period
common in those undergoing emergency surgery, of time has not been investigated. Nevertheless, it
prolonged cardiopulmonary bypass and those with would seem prudent to use them in all patients who
underlying lung disease, pulmonary hypertension, are reintubated following cardiac surgery as many of
renal disease or New York Heart Associate (NYHA) these patients stay on the ICU for prolonged periods
class IV heart failure. It is associated with a prolonged of time.
ICU stay and increased mortality. It is felt that pro- Selective digestive decontamination (SDD) is the
longed anaesthesia, hypothermia and underlying administration of broad spectrum antimicrobials
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Table 32.3 Possible strategies to reduce ventilator associated Table 32.4 Strategies recommended to reduce CLABSI
pneumonia
Hand hygiene prior to catheter insertion or manipulation
Semi-recumbent patient positioning
2% chlorhexidine skin preparation prior to line insertion
Appropriate stress ulcer prophylaxis
Strict maximal aseptic technique during line insertion
Oral decontamination with chlorhexidine
Avoid femoral access
Sedation interruptions
Remove all non-essential central lines
Subglottic suctioning
Disinfect hubs and injection ports prior to accessing the line
Selective digestive decontamination
in patients on cardiothoracic ICUs as it may result in

enterally to reduce the pathogenic flora of the intes-
endocarditis, infection of prosthetic valves and pacing
tinal tract. Aerobic Gram-negative organisms are tar-
systems.
geted particularly. Enteral agents include polymixin,
Many consider CLABSIs to be preventable.
colistin, tobramycin, nystatin and amphotericin
Multiple strategies (Table 32.4) can reduce the
that are poorly absorbed. They are combined with a
incidence of infection. The role of chlorhexidine
short course of broad spectrum systemic antimicro-
impregnated dressings and patches or antibiotic/
bials such as ciprofloxacin or a cephalosporin. Meta-
chlorhexidine/silver impregnated catheters is not clear.
analyses have demonstrated reduced rates of VAP
These strategies are often bundled together as a qual-
but concerns about the generation of multiantibiotic
ity improvement initiative. In Pronovost’s landmark
resistant infections have limited the adoption of SDD
study, this approach caused a sustained reduction in
into clinical practice. Two large international studies
rates by 66%, which was confirmed subsequently in
are planned (SuDDICO –clinicaltrials.gov reference
a randomised study. Globally, many countries have
NCT02389036; RGNOSIS –clinical trials.gov refer-
adopted this bundled approach.
ence NCY02208154) which may redress this clinical
Continuous monitoring of infection rates is
equipoise.
important for any ICU. A typical target would be less
Monitoring rates of VAP on an individual ICU
than 1 infection per 1000 catheter days, although data
are complicated by difficulties in the commonly used
collection is difficult and can vary between centres.
definition. Many rely on clinical signs and changes
The CDC has strict definitions of laboratory con-
in the chest radiograph which are subjective and
firmed infection but does not define the scenario of
not specific. The Centers for Disease Control and
suspected infection that could not be confirmed in the
Prevention (CDC) has recently described a clinical
laboratory. In practice many central lines are replaced
entity of ventilator associated events using objective
due to concerns about infection, although this is not
data that are relatively easy to collect electronically. In
subsequently proven even when the original concerns,
the setting of data suggesting infection then this may
such as elevated biomarkers of infection, are subse-
be upgraded to a diagnosis of VAP. The tools may be
quently allayed. Monitoring of suspected infection
useful for surveillance within a specific unit. Local
rates would probably be an additional metric in any
practices in ventilator setting can influence the rates,
quality improvement process.
making inter-hospital comparisons difficult, although
others have reported little inter- hospital variation
(Table 32.3). Surgical Site Infections
Sternal wound infections are a serious complication
Central Line Associated Blood Stream following cardiac surgery. Whilst superficial infec-
tions often increase length of stay in hospital, deep
Infections (CLABSI) infections are associated with substantial morbidity
Central venous access is frequently required in the and mortality. Deep infections are defined as those
cardiothoracic ICU for the administration of vasoac- that are associated with sternal dehiscence or infec-
tive agents, renal replacement therapy and the meas- tions down to the sternum even if the sternum is sta-
urement of cardiac output. Central line associated ble. Risk factors include diabetes mellitus, bilateral
blood stream infections are associated with increased mammary artery harvest, obesity, chronic obstruc-
mortality in patients. The consequences may be worse tive pulmonary disease, prolonged surgery, surgical
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re-exploration and delayed sternal closure for haemo- • Healthcare associated infections are common
dynamic compromise following cardiothoracic surgery, particularly
Strategies to prevent deep sternal infection include ventilator associated pneumonia, central line
preoperative skin care, prophylactic antibiotics prior associated blood stream infections and surgical
to the surgical incision and aseptic surgical technique. site infections. Clinicians can prevent many
Gentamicin impregnated sponges and beads have not of these infections and should measure their
been shown conclusively to reduce deep sternal infec- incidence as part of a quality assurance strategy.
tions and have not been adopted into routine practice. • Endocarditis is a challenging condition best
The management of deep sternal wound infections managed by a team of surgeons, cardiologists,
requires liaison between the cardiac surgeon, plas- microbiologists, intensivists and imaging experts.
tic surgeon and microbiologist. Coagulase negative
staphylococci (usually Staphylococcus epidermidis) are Further Reading
the most common aetiological organisms. Prolonged Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis
courses of antibiotics are often required and follow- Campaign: international guidelines for management
ing surgical debridement it is often necessary to fill the of severe sepsis and septic shock: 2012. Critical Care
defect with a myocutaneous flap such as a latissimus Medicine. 2013; 41: 580–637.
dorsi flap. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/
AHA/HRS 2008 Guidelines for Device-Based Therapy
of Cardiac Rhythm Abnormalities: a report of the
Conclusions American College of Cardiology/American Heart
Infection impacts on our patients. Avoiding healthcare Association Task Force on Practice Guidelines
associated infections is probably the greatest benefit (Writing Committee to Revise the ACC/AHA/NASPE
that we can afford our patients. Ventilator associated 2002 Guideline Update for Implantation of Cardiac
pneumonia and central line associated blood stream Pacemakers and Antiarrhythmia Devices): developed
in collaboration with the American Association for
infection are frequent and are avoided through pro-
Thoracic Surgery and Society of Thoracic Surgeons.
cesses of care. Circulation. 2008; 117: e350–408.
Broad spectrum antibiotics administered to
Habib G, Lancellotti P, Antunes MJ, et al. 2015 ESC
patients for prolonged periods of time promote Guidelines for the Management of Infective
the development of multidrug resistant organisms Endocarditis: The Task Force for the Management
and Clostridium difficile diarrhoea. Management of of Infective Endocarditis of the European Society of
infected patients centres around appropriate early Cardiology (ESC). Endorsed by: European Association
antibiotic therapy, source control and preservation of for Cardio-Thoracic Surgery (EACTS), the European
organ perfusion through the administration of intra- Association of Nuclear Medicine (EANM). European
Heart Journal. 2015; 36: 3075–3128.
venous fluids, intropes and vasoconstrictors.
He S, Chen B, Li W, et al. Ventilator-associated pneumonia
after cardiac surgery: a meta-analysis and systematic
Learning Points review. Journal of Thoracic and Cardiovascular Surgery.
• Many patients display significant systemic 2014; 148: 3148–3155, e3141–3145.
inflammation which manifests as vasoplegia, Michalopoulos A, Geroulanos S, Rosmarakis ES, Falagas
raised biomarkers and organ dysfunction ME. Frequency, characteristics, and predictors
following cardiothoracic surgery. It can be of microbiologically documented nosocomial
infections after cardiac surgery. European Journal of
difficult to determine whether concomitant
Cardiothoracic Surgery. 2006; 29: 456–460.
infection is a significant driver.
Pronovost P, Needham D, Berenholtz S, et al. An
• The Surviving Sepsis Campaign guides clinicians intervention to decrease catheter-related bloodstream
in the evidence-based management of patients infections in the ICU. New England Journal of
with sepsis and is usually equally applicable to Medicine. 2006; 355: 2725–2732.
patients with cardiorespiratory disease. Romero-Bermejo FJ, Ruiz-Bailen M, Gil-Cebrian J,
• Patients with cardiac dysfunction may not be Huertos-Ranchal MJ. Sepsis-induced cardiomyopathy.
able to increase their cardiac outputs to counter Current Cardiology Reviews. 2011; 7: 163–183.
vasoplegia. Their response to intravascular fluid Siempos II, Kopterides P, Tsangaris I, Dimopoulou
replacement may be different. I, Armaganidis AE. Impact of catheter-related
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bloodstream infections on the mortality of critically ill Septic Shock (Sepsis-3). Journal of the American
patients: a meta-analysis. Critical Care Medicine. 2009; Medical Association. 2016; 315: 801–810.
37: 2283–2289. Thuny F, Grisoli D, Collart F, Habib G, Raoult D.
Singer M, Deutschman CS, Seymour CW, et al. The Third Management of infective endocarditis: challenges and
International Consensus Definitions for Sepsis and perspectives. Lancet. 2012; 379: 965–975.
MCQs
1. Which of the following parameters have high sensitiv- (c) Uncontrolled infection
ity for infection in the first few days following cardiac (d) Prosthetic valve whose sewing ring is loose on TOE
surgery?
(e) Repeated cerebral emboli
(a) White blood cell count
4. Which is the best parameter to target during intrave-
(b) C-reactive protein nous fluid resuscitation of patients with cardiac dis-
(c) Pro-calcitonin ease and proven septic shock?
(d) All of the above ((a)–(c)) (a) Central venous/right atrial pressure
(e) None of the above ((a)–(c)) (b) Stroke volume
2. Regarding ventilator associated pneumonias, which of (c) Central venous oxygen saturations
the following interventions has NOT been shown to (d) Urine output
reduce the incidence in patients who have undergone
cardiac surgery? (e) Arterial lactate
(a) Semi-recumbent patient positioning 5. Which of the following parameters should be assessed
in infective endocarditis of the aortic valve?
(b) Daily change of ventilator circuit
(a) MIC of antibiotics for the organism
(c) Oral hygiene with 2% w/v chlorhexidine
(b) PR interval
(d) Avoidance of acid suppression therapies
(c) Blood cultures after a few days
(e) None of the above
(d) Only (a) and (b)
3. Which one of the following is NOT an indication for
expediting surgery in infective endocarditis? (e) All of the above ((a)–(c))
(a) Mitral regurgitation
(b) Heart failure, refractory to diuretics
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Seizures
Chapter
33 Ari Ercole and Lara Prisco
Introduction an important reversible cause of unconsciousness and

should be considered in the differential diagnosis of a
Seizures are common in intensive care patients gen-
patient who does not wake appropriately from seda-
erally and cardiac surgery or postcardiac arrest
tion or anaesthesia.
patients are at particular risk. Seizures are an impor-
Clinically apparent seizures are due to focal or
tant and potentially reversible cause of prolonged
global disorganised brain electrical activity and may
unconsciousness as well as being associated with
be manifest as changes in behaviour/level of con-
poorer ICU outcome, although the latter may be
sciousness or abnormal movements. However, in
multifactorial. Cerebral metabolic rate is greatly
sedated or critically ill patients, none of these find-
increased during seizure activity, which may lead to
ings may be clinically obvious or apparent. The diag-
energetic crisis and neuronal injury. Non-convulsive
nosis of true seizures is complicated by other types of
seizures are particularly common in ICU patients
abnormal movements that may be seen in intensive
and are under- recognised. Electroencephalography
care patients (such as shivering, myoclonus, tremor,
(EEG) is therefore an essential ICU investigation
emergence from neuromuscular blockade). A system-
for the diagnosis of seizures or epileptiform activity
atic approach to distinguishing seizures from non-sei-
and for distinguishing these from other disorders of
zure movements is helpful (Figure 33.1).
consciousness, which may have characteristic EEG
Most clinical seizures are self-limiting. Patients
signatures. Continuous EEG (cEEG) is particularly
will regain consciousness although a postictal period
sensitive for clinically occult seizures and is also help-
of altered mental state is common due to neurotrans-
ful for managing seizures refractory to simple treat-
mitter depletion, changes in receptor concentration/
ment. However, EEG requires specific expertise to
inhibition or altered cerebral blood flow. Sometimes
perform and interpret which can be a barrier to its use
clinical seizures may be prolonged or repeated. Status
in the cardiothoracic intensive care unit.
epilepticus (SE) is defined as ‘an acute epileptic condi-
tion characterised by continuous generalised convul-
The Burden and Characteristics of sive seizures for at least five minutes, or by two seizures
Seizures in Intensive Care without full recovery of consciousness between them’.
Seizures are common but under-recognised in the Electrographic seizure activity may also occur with-
ICU. Subclinical electrographic seizure activity is out movement, and this is particularly important in
common in neurosciences patients but may also occur ICU patients. Such non-convulsive seizures (NCS) are
in critically ill patients without a history of seizures. a more elusive diagnosis that is frequently unrecog-
Most studies show a prevalence of seizures of 15–40% nised. Its incidence after cardiac surgery is probably
and identify the presence of seizures and status epi- particularly high due to exposure of the patient to
lepticus as independent predictors of poorer outcome. some degree of subclinical embolic phenomena, met-
To what extent this represents a modifiable pathology abolic derangement, hypotension or proconvulsive
or an epiphenomenon of worse underlying neurologi- drugs. Non-convulsive SE (NCSE) is further defined
cal injury is uncertain. However, prolonged seizure as an electrographic diagnosis of ‘continuous or inter-
activity is associated with neuronal energetic failure mittent ictal discharges without the patient regaining
and injury. Therefore recognition and treatment of consciousness, and no overt clinical signs of convul-
seizures is important. Furthermore, seizures are also sive activity’. NCSE is often suspected in patients who
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Figure 33.1 The diagnosis and initial

Abnormal Movements after Cardiac Surgery management of seizures after cardiac
surgery. After Hunter and Young (2011), with
permission. VPA valproate; DPH phenytoin; SRU
seizures after cardiac surgery; LOC NYD altered
level of consciousness not yet diagnosed.
Seizure Other
Key features of history: Myoclonus
Head or eye deviation? Shivering
Tonic followed by clonic phase? Tremor
Postictal phase? Paralytics clearing
Duration? Posturing (severe global injury)
• Oxygenation, blood pressure management, draw bloodwork

• Lorazepam 2 mg IV if prolonged (>3–5 min), repeat as needed x 3
Withhold or decrease possible offenders
• Review meds (pre, intra and postoperative) and bloodwork, especially
Na+, Ca2+, Mg2+, renal function
• Stat EEG (or bedside EEG system if full EEG unavailable)
Generalised
• CT reasonable, not always necessary, especially if
improving and generalised S+W on EEG
• Short-term (3–5 days) VPA probably most effective,
DPH often used due to familiarity
• Concerns with DPH in CSRU re:
bradycardia/block, hypotension requires long
infusion time
Focal
• CT or MRI based on availability and patient stability
• DPH or VPA reasonable options with above limitations still
applicable
• If persistent decreased LOC NYD or subtle signs
suggesting NCSE (facial twitching, nystagmus, etc) obtain
full 10–20 EEG
• Management dependent upon test results
were in convulsive SE and subsequently do not fully and clinically suspected NCSE. Studies prospectively
regain consciousness. Hence, if coma persists after SE, performing EEGs in unselected comatose patients
EEG is necessary to identify the cause of unconscious- without clinical signs of seizures found either NCS or
ness (NCSE or a postictal state). However, it may NCSE in up to 8% of cases.
occur de novo in ICU patients and this represents a
particular diagnostic challenge. Electroencephalography
NCS have been reported in up to 37% of criti- Given the diagnostic difficulties presented by criti-
cally ill patients undergoing cEEG monitoring. The cally ill patients, the unequivocal detection/exclusion
highest proportion of NCS is seen in patients who of seizures often requires EEG. This is a technique that
underwent emergency EEGs for altered mental status measures the spatial distribution of voltage fields on
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Chapter 33: Seizures
nasion
Nz
left Fpz right

Fp1 Fp2
F7 F3 F4 F8
Fz
T3 C3 Cz C4 T4
P3 Pz P4
T5 T6
O1 Oz O2
Iz
inion
Figure 33.2 Left panel: typical EEG scalp electrodes for clinical use. Right panel: international 10–20 system for standard scalp electrode
placement. The distances between adjacent electrodes are either 10% or 20% of the total anterior/posterior or left/right distance. Left and right are
distinguished by odd and even numbers respectively. Each channel of the EEG is obtained by measuring the voltage between adjacent electrodes
(bipolar montage, such as here) or of individual electrodes compared to a reference electrode or combination of electrodes (referential montage).
(A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)
the scalp and their variation over time. The origin of symmetry, synchrony, reactivity (to external stimula-
this activity is thought to reflect the fluctuating sum of tion), morphology, rhythmicity and regulation. The
excitatory and inhibitory postsynaptic potentials that signal frequencies detected by a standard clinical EEG
arise primarily from apical dendrites of pyramidal are divided into four standard frequency ranges or
cells in the outer layer of the cerebral cortex under the ‘bands’: alpha (8 to <13 Hz, usually occipital), beta
input from subcortical structures. (>13 to 25 Hz, usually frontal and central), theta (4
The potentials recorded by the EEG are very small to <8 Hz, usually central or diffuse) and delta (<4 Hz,
(of the order of microvolts) and are therefore eas- focal or diffuse).
ily contaminated by electrical noise and other arte- The most important EEG pattern of wakeful-
facts such as the electromyogram when trying to ness is a posterior dominant rhythm (PDR). The
record from areas with larger underlying muscles. PDR is located predominantly at the occipital poles
Furthermore, EEG changes may be relatively local- but becomes anterior as the patient becomes drowsy
ised, meaning that an array of electrodes is needed to (normal sleep). This activity is normally in the alpha
cover the whole scalp adequately. Finally, seizures may range and is symmetrical. Slower rhythms such as
occur intermittently and so continuous recordings generalised continuous delta are always abnormal and
(cEEG) over 12–24 hours or even longer are needed are usually associated with diffuse or multifocal cor-
to realise the highest diagnostic sensitivity. Such con- tical injury or metabolic derangement. Intermittent
siderations make recording a clinically useful EEG slowing, such as intermittent rhythmic delta activity
much more complex and involved than, say, an ECG. (IRDA) and frontal IRDA (FIRDA) or occipital IRDA
The American Clinical Neurophysiology Society has (OIRDA) are thought to be caused by dysfunction in
published recommendations for recording ICU cEEG. subcortical centres influencing cortical activation and
Equipment, length of recording and electrode mon- may represent a manifestation of a more generalised
tages should meet the technical standards defined in process not limited to the frontal or occipital lobes.
these consensus statements (Figure 33.2). Reactivity refers to a clinical (electromyographic
Even in the absence of seizures, the EEG shows activity, respiratory pattern change) and/ or EEG
stereotypical changes with consciousness, which can response (increased continuity, amplitude reduc-
be diagnostically useful. EEG activity can be classi- tion, frequency change) to external stimulation (pain,
fied by frequency, amplitude, distribution or location, passive eyes opening, auditory stimuli). In cardiac
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arrest patients, a non-reactive EEG background after or the camera of the EEG acquisition unit. Routine
rewarming is associated with poor neurological out- ICU care such as physiotherapy, suctioning and oral
come. However, the association is complex: this pat- care can create rhythmic artefacts that mimic electro-
tern is still compatible with good recovery when graphic seizures but are easily identified with video
observed during therapeutic hypothermia and analysis.
patients with myoclonus and no EEG reactivity within EEG electrode technology is sophisticated. The
72 hours from cardiac arrest have occasionally gone low voltages involved mean that very low electri-
on to have good outcomes. cal impedances are required. Poor contact renders
Electrographic seizures are characterised by repet- the electrodes susceptible to electrical interference.
itive or rhythmic focal or generalised epileptiform dis- Electrical noise from intravenous pumps, electrical
charges at greater than 3 Hz, and lasting more than 10 beds, dialysis machines and other medical devices can
seconds or at less than 3 Hz but with clear evolution obscure the EEG recording and requires proper iden-
in frequency, location, waveform or field or clinical tification and trouble-shooting.
manifestation. They usually resolve or improve after Specialised hardware and software increase the
administration of rapid acting intravenous antiepilep- utility of cEEG for monitoring at the bedside. Options
tic drugs such as benzodiazepines. The electrographic include the ability to enter nursing notes, pushbuttons
features of SE are highly variable, including rhyth- for seizures and other clinical events, software to inte-
mic, generalised and symmetric spike-and-waves or grate physiological data, and quantitative EEG soft-
polyspikes-and-waves at 2 to 3.5 Hz, or atypical spike- ware for graphical display of quantitative EEG trends.
and-wave with lower frequency and less symmetry, or
multiple spike-and-wave, or high voltage, repetitive, Causes and Prognostic Significance of
rhythmic (focal or generalised) delta activity with
interspersed spikes, sharp waves or sharp components
Seizures in Intensive Care
(Figure 33.3). The dominant aetiology and prognostic significance
If continuous EEG is not available, multiple inter- of seizures in the cardiothoracic intensive care unit
mittent serial recordings are desirable as seizures varies from patient to patient. Three distinct patient
may otherwise be missed, especially as high dose populations are of particular importance in the car-
anaesthetics are weaned. Whilst the EEG does not diac ICU: those who are post cardiac surgery (where
change significantly at body temperatures between embolic phenomena are likely to be important),
32 and 34°C, sedative drugs commonly used during patients successfully resuscitated from cardiac arrest
therapeutic hypothermia can markedly affect the EEG (where hypoxic- ischaemic injury dominates) and
background. those patients suffering from general critical illness.
Regular electrode maintenance, scalp inspec-
tions, keeping the scalp dry and reducing pressure on Postcardiac Surgery
the scalp from the electrodes is important to avoid Postoperative seizures are known to complicate car-
scalp injuries. Sweating and scalp breakdown are diac surgery with an incidence of up to 7% and recur-
more common in patients with fever, sepsis and pro- rence rates of around 50%. This is almost certainly an
longed systemic disease requiring frequent changes underestimate, with NCS probably frequently missed
of electrodes. Hypothermia presents a theoretically and not necessarily benign. The manifestations and
increased risk of coagulopathy. However, scalp break- causes of seizures in the context of cardiac surgery are
down with bleeding or infection has not been reported diverse, as are the expected outcomes. Both convulsive
among postarrest patients treated with therapeutic and non-convulsive seizures may contribute to pro-
hypothermia (even up to several days of cEEG with longed reduced levels of consciousness, an increased
either disposable or reusable versions of disc elec- length of stay in the ICU, and a possible increase
trodes, Figure 33.2). in morbidity and mortality. Furthermore, convulsive
The EEG is typically recorded for later off-line seizures lead to cardiovascular strain and metabolic
analysis by a neurophysiologist. To this end the use derangement in patients already in a fragile state.
of simultaneous video recording is recommended Perioperative seizures may be caused by throm-
to identify sources of artefact and must be correctly boembolic ischaemic stroke, cerebral air embolism,
repositioned when the staff moves either the patient antibiotic toxicity or other perioperative drugs such as
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Fp2 F8 Fp2 AVG
F8 T4 Fp1 AVG
F8 AVG
T4 T6
F4 AVG
T6 O2 Fz AVG
FP2 F4 F3 AVG
F4 C4 F7 AVG
T4 AVG
C4 P4
C4 AVG
P4 O2
Cz AVG
Fp1 F3 C3 AVG
F3 C3 T3 AVG
T6 AVG
C3 P3
P4 AVG
P3 O1
Pz AVG
Fp1 F7
P3 AVG
F7 T3 T5 AVG
T3 T5 O2 AVG
Normal O1 AVG
Encephalopathy
T5 O1
ECG
ECG
S/W P3
Fp2 F8 Fp2 F8
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F8 T4 F8 T4
T4 T6 T4 T6
T6 O2 T6 O2
FP2 F4 FP2 F4
F4 C4 F4 C4
C4 P4 C4 P4
P4 O2 P4 O2
Fp1 F3 Fp1 F3
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F3 C3 F3 C3
C3 P3 C3 P3
P3 O1 P3 O1
Fp1 F7 Fp1 F7
F7 T3 F7 T3
T3 T5 T3 T5
T5 O1 SE T5 O1
LPD
ECG ECG
Figure 33.3 Examples of EEGs from the ICU. Top left: normal wakeful EEG, high frequencies with alpha wave activity dominant in posterior/occipital channels. Top right: encephalopathic EEG
illustrating prominent slow (delta wave) activity. Bottom left: generalised seizure activity with sharp spikes and waves in all channels. Bottom right: LPDs, periodic spike discharges over the left
hemisphere (odd numbered channels). (A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate section.)
290
tranexamic acid (TXA). Several risk factors have been 3 to 5 days after cardiac arrest. It is important to appre-
directly associated with the presence of postopera- ciate that although rare (less than 5%) there have been
tive seizures. Open-chamber procedures, including reports of survivors of MSE with good cognitive out-
valve and aortic repairs and cardiac transplants, have come. Most of these patients were treated with at least
a higher incidence of complications than does coro- three to four antiepileptic drugs (including high dose
nary artery bypass graft surgery. The combination of anaesthetics), had preserved brainstem reflexes, intact
TXA administration, especially high doses (>80 mg/ cortical somatosensory evoked potential responses
kg) and open-chamber surgery has been confirmed and reactive EEG backgrounds.
in several studies as an important perioperative fac- Subcortical structures are involved in MSE and
tor. Higher preoperative creatinine (>120 μmol/l), therefore the EEG does not show the same electro-
thoracic aortic surgery and early seizures onset (<4 graphic features. Instead the EEG may show gen-
hours) have also been found to increase risk of recur- eralised periodic discharges (GPDs) and/or a burst
rent seizures (RS). Despite longer ICU stay and dura- suppression pattern. A brainstem origin of postanoxic
tion of mechanical ventilation, the presence of RS is myoclonus may be suspected when there is sequen-
not associated with significantly increased long-term tial activation of muscles innervated by cranial nerves
morbidity or mortality. (reticular reflex myoclonus) and characterised by
non-specific EEG changes (non-epileptiform patterns
Postcardiac Arrest such as diffuse alpha activity). By contrast, cortical
action-reflex myoclonus instead presents with epilep-
Clinical seizures occur in up to 40% of patients fol-
tiform discharges and/or polyspikes and typically (but
lowing cardiac arrest, mostly in the first 3 to 5 days.
not necessarily) affects a few muscles in a localised
Seizures most commonly present as diffuse or mul-
distribution.
tifocal myoclonus or focal and generalised tonic-
MSE may be confused with chronic post-hypoxic
clonic seizures, and contribute to decreased level of
myoclonus (Lance–Adams Syndrome, LAS). LAS is a
consciousness; they have important implications for
distinct entity that may also appear after a period of
prognosis.
cerebral hypoxia in patients with a more prolonged
Non-convulsive seizures may occur and often pre-
coma or period of sedation. In contrast to MSE, LAS
sent as NCSE.
develops later, days or weeks after the initial hypoxic
NCSE after cardiac arrest is very difficult to treat,
event, and does not respond to anticonvulsant treat-
and it is not clear if treatment improves neurological
ment. Crucially, however, such patients regain con-
outcome or mortality. However, it is common: post-
sciousness, but may exhibit muscle jerks affecting face,
arrest patients treated with therapeutic hypothermia
trunk or limbs often provoked by sensory stimuli and
and receiving routine EEG or cEEG monitoring have
strikingly elicited by the willed voluntary action. LAS
a prevalence of NCSE/SE of around 30%. Clinical sei-
is rare, but its differentiation from MSE is important
zures typically begin within the first 2 days following
to avoid incorrect prognostication and for the institu-
cardiac arrest but it is not uncommon to see earlier
tion of timely rehabilitation.
electrographic seizures on the EEG. Several studies
have shown that initial electrographic seizures are
typically not associated with any clinical correlate of General Intensive Care Considerations
myoclonus or other motor seizure types by day 2 to 3. In the cardiac ICU, anoxic brain injury is a com-
Myoclonus can also occur in patients with hypoxic mon cause of severe encephalopathy as well as sei-
brain injury and may be either acute or chronic. Acute zures, and ischaemic or haemorrhagic stroke must
post-hypoxic myoclonic status epilepticus (MSE) be suspected in patients who had cardiac surgery
occurs soon after a hypoxic insult and is a clinical and develop postoperative seizures or SE. However,
diagnosis consisting of unrelenting diffuse myoclonus there are many possible causes for seizures in the
involving the face, limbs and torso that is often precipi- critically ill and a single cause may often never be
tated by stimulation. It is strongly associated with poor identified.
outcome if onset is during the first 24 hours postar- Sepsis is the most frequent cause of altered mental
rest, and this association remains true with therapeutic status in the general ICU as sepsis related encepha-
hypothermia, although the onset may be delayed until lopathy has been associated with neuronal damage,
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291
mitochondrial and endothelial injury, and distur- given followed by a loading dose of phenytoin (20 mg/
bances in neurotransmission. Metabolic alterations kg infused at a maximum rate of 50 mg/minute).
due to hepatic and/or renal dysfunction can lead to a A significant minority of patients with SE may be
background of encephalopathy. refractory to adequate doses of two AEDs. If SE has not
Other primary systemic diseases can present as responded to this first line treatment and lasts 60–90
altered mental status and are associated with seizures minutes, patients will risk physiological compromise,
(such as posterior- reversible leukoencephalopathy neuronal damage and increasing drug resistance. The
secondary to malignant hypertension, eclampsia, patient should be anaesthetised and transferred to the
metabolic and electrolyte disturbances, embolic cer- ICU to stop seizure activity. Propofol is likely to be the
ebral infarcts or mycotic aneurysms from endo- most familiar agent and is an effective anticonvulsant,
carditis, central nervous system vasculitis from an although midazolam may be employed. More rarely
underlying autoimmune disease such as polyarteritis barbiturates such as thiopentone may be required but
nodosa, systemic lupus erythematosus, and Sjøgren’s specialist advice should be sought.
syndrome, paraneoplastic syndromes and limbic Laboratory tests to pursue include the follow-
encephalitis). ing: blood glucose, full blood count, metabolic profile,
Transplant patients in the postsurgical ICU are liver function test, magnesium, phosphate, urine toxi-
another population at risk for altered mental sta- cology, serum ethanol levels, troponin, creatine kinase
tus and seizures. Seizures in these patients are often (CK), urinalysis, urine and blood cultures, and AEDs
multifactorial with causes including severe meta- levels. If vitamin B1 deficiency is suspected (history of
bolic derangements, toxicity from immunosuppres- dietary insufficiency/inadequacy), intravenous thia-
sive therapy, and other postoperative complications. mine should be administered before giving glucose
Central nervous system infections are an important to avoid precipitation of Wernicke’s encephalopathy.
cause of seizures, and this is of particular significance Acid-base alterations and hyperthermia are common
in patients who are immunosuppressed. during SE and should be treated as soon as possible.
A degree of rhabdomyolysis is common and can lead
to acute kidney injury or even renal failure. Depending
Management of Seizures on CK levels, urine output should be maintained and
SE is an emergency and must be treated aggressively alkalinisation with intravenous sodium bicarbonate
and early as the longer an episode of SE persists, the considered. If CK is severely elevated, then renal
more refractory the patient will become to treatment. replacement should be commenced from the outset to
Also, clinically evident seizures should be treated remove circulating myoglobin, although this is rare in
immediately without waiting for the EEG but cEEG the context of seizures alone.
should ideally be started if a patient requires continu- A CT head scan must be performed once the
ous neuromuscular blockade after initial treatment patient is stabilised and clinically apparent seizures
with antiepileptic drugs (AEDs). have stopped. If the aetiology is unknown and the
It is important to assess and manage the patient’s CT head scan is negative, an MRI head scan should
airway because apnoea or airway soiling can occur be performed. In patients with SE of unknown ori-
with generalised seizures and intubation may be gin, a lumbar puncture is indicated and empirical
required. The use of short-acting paralytics is prefera- cover with CNS-penetrating antibiotics and antivirals
ble for intubation so that on-going seizure activity will should be considered while CSF analysis, microscopy,
not be masked. Autonomic instability may accompany culture and PCR studies are being obtained. This is
seizures and cardiovascular support may be required. particularly important in febrile or immunocompro-
Once SE has become established, rapid adminis- mised patients.
tration of intravenous therapy is required to control Phenytoin has gained widespread acceptance as
seizures. Whilst any benzodiazepine may be effective, a first line antiepileptic drug (AED) due to its avail-
lorazepam is the drug of choice as it has a long redis- ability, intravenous formulation, effectiveness and
tribution half-life (3–10 hours) reducing the likeli- familiarity. However, its use in the cardiac intensive
hood of rebound seizures. If the first bolus (usually care unit must be carefully considered. In patients
2–4 mg in adults) fails, then a second bolus can be with postcardiac arrest SE and after cardiac surgery,
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292
special attention should be given to the risk of cardiac Laboratory barbiturate assay is possible but not locally
dysrhythmia (bradycardia occasionally progressing to available in most hospitals.
heart block) or hypotension in this very susceptible Once the patient has been sedated, EEG (ideally
population. In addition, phenytoin and warfarin have cEEG) is helpful in establishing on-going AED effec-
complex and poorly understood interactions that vary tiveness, whether a second AED is needed and what
with cytochrome p450 genetic polymorphisms, which maintenance therapy will be required after sedation
may limit its use in patients requiring anticoagulation. withdrawal. Once all seizure activity has stopped for
Phenytoin has a long half-life and dosing must be more than 24 hours, and provided there are adequate
carefully considered. It is also strongly protein bound blood levels of AEDs, then the anaesthetic can be
and levels should be checked regularly and be adjusted slowly weaned. Should SE recur, other drugs may be
for serum albumin levels to avoid inadvertent overdose: tried, but good clinical trials are lacking to date.
[Corrected phenytoin] = [Measured phenytoin] /
(0.29 × Albumin + 0.1). Seizures versus Epileptiform
For CrCl <10 ml/minute or in renal replacement Activity: To Treat or Not To Treat?
therapy use: In addition to definitive seizure activity, the EEG may
[Corrected phenytoin] = [Measured phenytoin] / also reveal abnormal epilepsy-like activity. Although
(0.1 × Albumin + 0.1). strictly speaking such epileptiform discharges are not
seizures, they may be important as their presence is
Valproate is an alternative to phenytoin. It is not highly associated with both convulsive and non-
associated with significant cardiac side effects, can be convulsive seizures. Periodic discharges (PDs) are
loaded quickly intravenously (30 to 60 mg/kg infused stereotyped repetitive discharges with diverse elec-
over 30 to 60 minutes followed by maintenance 15 to trographic morphology that occur at regular intervals
20 mg/kg in divided doses) and is very well tolerated. and may be localised to one hemisphere (lateralised
It is hepatically metabolised but is safe even in patients PDs, LPDs) (Figure 33.2) or bilateral (bilateral inde-
with mild to moderate liver dysfunction. Valproate pendent PDs, BIPDs and generalised PDs, GPDs).
has been demonstrated to be at least as effective as The clinical significance and management of epi-
phenytoin in treating SE. A rare side effect that must leptiform activity is controversial, especially in coma-
be suspected in prolonged recovery after seizures in tose patients. In the general ICU more than 20% of
patients loaded with valproate is hyperammonaemia, patients are estimated to suffer electrographic seizures
an idiosyncratic metabolic response. or PDs. The presence of PDs is associated with a higher
Another option that is gaining popularity in all incidence of death or severe disability at hospital dis-
ICU settings is levetiracetam, due to its minimal charge; however, the clinical significance of PDs and
drug– drug interactions and unchanged excretion their association with underlying structural injury are
such that hepatic disease does not preclude its use. The still controversial. Whether epileptiform activity is
dose should be adjusted in renal failure to allow for a true interictal pattern or instead simply represents
decreased clearance. A starting dose of 500 mg twice a predisposition to seizures is unclear. Evidence for
a day is thought to achieve therapeutic levels in most improvement in outcome from treatment with AEDs
patients, although this may rapidly be increased over a is lacking. Nevertheless these patterns are pathologi-
few days to 1500 mg twice daily if required. Valproate, cal: the clinical significance and management of such
benzodiazepines and levetiracetam have shown some epileptiform findings should therefore be considered
efficacy in reducing postanoxic myoclonus. on a case-by-case basis.
In the rare situations where moderate or high
doses of barbiturates have been used, any neuro-
logical prognostication should be delayed because of Learning Points
their prolonged sedative effect. A randomised trial of • Seizures are common in both the general ICU and
refractory SE found a median duration of intubation cardiac ICU in particular. Seizures are associated
of 14 days in survivors in the thiopental or pento- with poorer outcomes.
barbital infusion arm, versus 4 days for survivors in • Seizures are an important reversible cause of
the propofol arm with no differences in mortality. unexplained unconsciousness.
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• Many seizures in the critically ill are non- Hosokawa K, Gaspard N, Su F, et al. Clinical
convulsive and therefore may go unrecognised. neurophysiological assessment of sepsis-associated
• Electroencephalography is required for the brain dysfunction: a systematic review. Critical Care.
2014; 18: 674.
diagnosis of seizures and a range of seizure-like
pathologies. Hunter GR, Young GB. Seizures after cardiac surgery.
Journal of Cardiothoracic and Vascular Anesthesia.
• EEG equipment is complex to set up and 2011; 25: 299–305.
interpretation requires specialist expertise.
Kalavrouziotis D, Voisine P, Mohammadi S, Dionne
S, Dagenais F. High-dose tranexamic acid is
Further Reading an independent predictor of early seizure after
cardiopulmonary bypass. Annals of Thoracic Surgery.
Chen JW, Wasterlain CG. Status epilepticus:
2012; 93: 148–154.
pathophysiology and management in adults. Lancet
Neurology. 2006; 5: 246–256. Oddo M, Carrera E, Claassen J, Mayer SA, Hirsch LJ.
Continuous electroencephalography in the medical
Claassen J, Mayer SA, Kowalski RG, Emerson RG,
intensive care unit. Critical Care Medicine. 2009;
Hirsch LJ. Detection of electrographic seizures with
37: 2051–2056.
continuous EEG monitoring in critically ill patients.
Neurology. 2004; 62: 1743–1748. Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S,
Fugate JE, Wijdicks EF, Mandrekar J, et al. Predictors of Quality Standards Subcommittee of the American
neurologic outcome in hypothermia after cardiac Academy of Neurology. Practice parameter: prediction
arrest. Annals of Neurology. 2010; 68: 907–914. of outcome in comatose survivors after
cardiopulmonary resuscitation (an evidence-based
Herman ST, Abend NS, Bleck TP, et al. Consensus review): report of the Quality Standards Subcommittee
statement on continuous EEG in critically ill of the American Academy of Neurology. Neurology.
adults and children, part II: personnel, technical 2006; 67: 203–210.
specifications, and clinical practice. Journal of Clinical
Neurophysiology. 2015; 32: 96–108.
MCQs
1. Any seizure lasting longer than what period of time is (c) Stroke
defined as status epilepticus? (d) All of the above
(a) 1 minute 4. Which one of the following regarding neurological
(b) 5 minutes outcome after cardiac arrest is true?
(c) 30 minutes (a) The Lance–Adams syndrome is associated with a
(d) 60 minutes good neurological outcome
2. When we are awake and very alert, the EEG normally (b) It can be predicted at 24 hours in patients who have
shows: undergone therapeutic hypothermia
(a) Beta waves (13–30 Hz) (c) Targeted-temperature management to 36 °C is not

associated with better neurological outcome
(b) Theta waves (5–7 Hz)
(d) EEG/cEEG should be recorded only in patients
(c) Alpha waves (8–12 Hz) with clinical signs of seizures/SE
(d) Delta waves (1–4 Hz) 5. Which of the following is the drug of first choice in a
3. Which one of the following cardiac surgery risk fac- patient with generalised convulsive status epilepticus?
tors would be more likely to be present in patients (a) Propofol
with postoperative seizures?
(b) Phenytoin
(a) High doses of tranexamic acid
(c) Pentobarbital
(b) Open-chamber procedures
(d) Lorazepam
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The Acute Abdomen in the Cardiac

Chapter
Simon JA Buczacki and Justin Davies
Introduction • Liver failure

• Myocardial infarction.
Abdominal complications following cardiothoracic sur-
gery are infrequent (0.3–5.5%) but carry a significant Although extended CPB times are associated with
mortality rate of around 30% (14–63%). This figure is elevated risk, the issue of whether off-pump CABG
far greater than is seen with the same pathologies in the (OPCABG) is protective has been extensively debated
general population, suggesting the physiological changes in the literature. A study reported in 2003 by Raja
imparted by cardiothoracic surgery have a major and et al. suggested that OPCABG decreased the incidence
deleterious result in the body’s ability to respond to of gastrointestinal complications from 7.3% to 0.6%.
abdominal pathology. Many of the abdominal complica- These results, however, have failed to be replicated by
tions discussed, such as mesenteric ischaemia, can have other groups; indeed it has further been shown that
subtle initial presentations where early intervention can during OPCABG when accessing difficult to reach
have the most benefit to prevent abdominal catastrophe. coronaries, the superior mesenteric artery blood sup-
These findings suggest there should be a high index of ply is disturbed. General consensus currently is that
suspicion for abdominal pathology in the postoperative OPCABG is not protective but the question remains
cardiothoracic patient who is failing to progress in the to be definitively answered.
intensive care environment. Although not designed specifically for this pur-
pose, EuroSCORE has been used to predict the
Risk Factors and Prediction development of gastrointestinal complications. An
Large retrospective and prospective studies have alternative scoring model termed the gastrointestinal
identified several risk factors for the development of complication score (GICS) has been developed with
abdominal pathology after cardiothoracic surgery: the aim to more accurately predict the development
• Old age (>70 years) of these pathologies. Using prospective collection of
• Low cardiac output (secondary to AF data from over 5500 patients, the authors identify that
or congestive cardiac failure) those with a GICS of ≥15 have a probability of devel-
• Peripheral vascular disease oping GI complications of >20% whereas a score of ≤5
• Reoperation secondary to haemorrhage has a probability of <0.4%. The authors identify sev-
• Renal failure (chronic and acute) eral independent predictors of these complications,
which are weighted accordingly (Table 34.1).
• Prolonged cardiopulmonary bypass (CPB) time
The GICS has been tested on a validation set of over
(>150 minutes)
1000 patients and is reported to have a sensitivity of 56%
• Use of an intra-aortic balloon pump
and a specificity of 88% for a GICS of 5; and a sensi-
• Preoperative inotropic support
tivity of 13% with a specificity of 99.8% when the score
• Active smoker is ≥15. GICS had a larger area under the curve than
• Chronic obstructive pulmonary disease EuroSCORE when receiver operating characteristic
• Prolonged ventilation (ROC) curve analysis was performed, although of note
• Valve surgery this only reached statistical significance in the devel-
• Sepsis opmental data set. Overall, GICS appears to provide a
• Deep sternal infection useful adjunctive tool to help identify patients at risk of
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Chapter 34: The Acute Abdomen
postoperative gastrointestinal complications. Although cardiothoracic ICU are more susceptible due to the
GICS is useful in predicting which patients may develop common use of antiplatelet agents and also instrumen-
abdominal complications, the nature of the pathologies tation of the upper GI tract with transoesphageal echo
is such that prophylactic measures introduced in those (TOE). The patient with an upper GI bleed may pre-
with high scores are unlikely to be of benefit. sent with frank haematemesis, cardiogenic shock or
melaena. It is important not to forget that a significant
Incidence of Abdominal Complications upper GI bleed can present solely with fresh blood per
Abdominal complications after cardiac surgery are rectum, thereby mimicking a lower GI bleed. Upper
not common, although the associated risk of mortal- GI bleeds can cause elevations in serum urea levels as
ity is great (Table 34.2). In addition to the postopera- well as the more characteristic drop in haemoglobin.
tive pathologies described below, it is important not to Abdominal signs are often lacking and tenderness is
forget that common causes of the acute abdomen in the normally absent. After resuscitation and correction of
general population can also, coincidentally, occur in the any clotting abnormalities, the first line investigation
patient after cardiac surgery. These can include adhesive in any significant GI bleed is an upper GI endoscopy to
small bowel obstruction, incarcerated/strangulated her- exclude a bleeding peptic ulcer or alternative upper GI
niae, appendicitis or pyelonephritis to name but a few. pathologies such as oesophageal varices. Should a pep-
tic ulcer be identified, dual-modality therapy is recom-
mended with the options including adrenalin injection,
Diagnosis and Management of the clips or diathermy. High dose proton pump inhibitor
Common Intra-abdominal Complications therapy should be commenced and Helicobacter pylori
eradication therapy started if biopsy (CLO test) results
Gastrointestinal Haemorrhage confirm infection. Should the patient suffer a rebleed
The vast majority of postoperative gastrointesti- after primary endoscopy, the options are either repeat
nal bleeds are from the upper gut. Patients in the endoscopy, interventional radiology (IR) with pos-
sible embolisation of the bleeding vessel (usually the
gastroduodenal artery) or if these fail, surgery. Surgery
Table 34.1 Gastrointestinal complication score (GICS) involves an upper midline laparotomy and under-
Postoperative vascular complication 9.5 running of the bleeding vessel following enterotomy.
Preoperative inotropic support 4.0 Alternative diagnoses such as bleeding oesophageal
Postoperative heart failure 3.5
varices can be managed endoscopically with the appli-
cation of ligation rubber bands in conjunction with
Reoperation for haemorrhage 3.5
medical control of portal venous hypertension.
Age >80 years 2.5
Significant lower GI bleeds which fail to stop early
Current smoker 2.5 with resuscitation and correction of clotting abnor-
Cardiopulmonary bypass >150 minutes 2.5 malities can be extremely difficult to manage.
Postoperative atrial fibrillation 2.5 The use of adjunctive medical therapies can be
NYHA class III–IV 2.0 helpful in these situations, in particular intravenous
tranexamic acid can, on occasion, slow down or
Table 34.2 Approximate incidence and mortality rates of common postoperative abdominal

complications (data from Rodriguez et al., 2010)
Incidence Mortality
Gastrointestinal bleed (upper GI (90%) lower GI (10%)) 0.39 19
Ischaemic bowel 0.16 50
Pancreatitis 0.13 20
Acute cholecystitis 0.11 27
Perforated peptic ulcer 0.07 36
Pseudo-obstruction 0.06 50 (with perforation)
Diverticulitis 0.03 21
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296
even stop significant colonic bleeds. It is imperative commonly only occur late. However, in the sedated
in situations of massive rectal bleeds to first exclude patient the suggestion of non- occlusive ischaemia
an upper GI bleed by endoscopy as well as bleeding can be subtle, varying from increasing nasogastric
haemorrhoids by using bedside proctoscopy. Should outputs, diarrhoea ± blood or a slowly rising unex-
these tests fail to identify a source for the bleed and plained metabolic acidosis in combination with raised
if the patient is generally haemodynamically stable, serum lactate. In the stable patient, the investigation
then a CT angiogram should be obtained. In order of choice if mesenteric ischaemia is suspected is a
for this investigation to successfully identify a bleed- contrast enhanced CT scan. Endoscopy (both upper
ing point, the patient needs to be bleeding at a rate and lower) can also be performed if CT is equivocal.
of >0.5 ml/minute. However, if a location is identified Ultimately, however, laparotomy is not uncommonly
this facilitates the possibility of an IR approach using used as a diagnostic tool in sick patients, and should
conventional angiography in conjunction with embo- be considered in a patient where there is a high risk of
lisation. In the absence of IR, CT angiogram can still clinical suspicion for mesenteric ischaemia even if the
be of help as it can direct targeted therapeutic colo- CT scan is non-diagnostic.
noscopy or surgical resection. If the bleeding patient In non- occlusive mesenteric ischaemia, prior-
is more unstable, or if CT angiogram fails to identify ity should be given to resuscitation and improve-
a bleeding location, the next option is therapeutic ment of cardiac output once the diagnosis is made or
colonoscopy which can be performed in the operating suspected. If the clinical picture progresses and the
theatre. Careful wash-out and mucosal inspection can patient deteriorates then laparotomy may be the only
permit diagnosis and therapeutic intervention, with option for survival.
the use of clips and/or adrenaline injection to achieve In both occlusive and non-occlusive mesenteric
haemostasis. In the case of a patient continuing to ischaemia it is not uncommon to find the entire intes-
bleed profusely and no active bleeding site identified, tine may be non-viable. Depending on the amount
the endoscopy can be augmented by a laparotomy to of intestine and other associated viscera that have
aid wash-out of the colon through the appendix, and infarcted, the surgical options are either resection
should the colon be cleared as a source of bleeding, with stoma formation accepting the high likelihood
sequential enterotomy and small bowel endoscopy to of lifelong parenteral nutrition dependency or ‘open-
identify the site can then be undertaken. However, and-shut’ where the degree of ischaemia is extensive
undertaking a laparotomy when the site of bleeding and not compatible with ongoing life.
is not known in advance should be avoided whenever
possible. Hepatobiliary (HPB) Complications
Mesenteric Ischaemia Pancreatitis
Postoperative mesenteric ischaemia carries a very As with all the other pathologies here described, the
high mortality rate. Two forms of ischaemia are mortality rate from pancreatitis in this patient cohort
described: occlusive and non- occlusive. Occlusive (20%) exceeds that of pancreatitis in the general popu-
disease occurs as a result of migration of emboli or lation (5%). However, the management of the condi-
the development of de novo thrombus. Non-occlusive tion follows the same principles. As with mesenteric
disease is more common in this patient group and ischaemia, the diagnosis of pancreatitis can be difficult
develops secondary to hypoperfusion from low car- as the symptoms and signs can be impossible to elicit
diac output or the use of vasoconstrictors. Occlusive in the sedated patient. The aetiology of pancreatitis
ischaemia tends to follow a very rapid course with here is more commonly secondary to reduced perfu-
the development of acidosis and ultimately intestinal sion although the possibility of ‘traditional’ gallstone
infarction. Non- occlusive disease generally follows pancreatitis should not be dismissed.
a slower clinical trajectory and in the intubated and An elevated serum amylase level is reportedly
sedated patient can be problematic to diagnose. In the present in 30–40% of all patients following cardiac
awake patient, pain, nausea/vomiting and bloody diar- surgery, although only 1–3% of these will have pan-
rhoea can be present with the pain classically being creatitis. Elevated serum lipase levels can be used
‘out of proportion’ to the abdominal signs, which to aid the diagnosis but do not appear to confer any
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297
additional sensitivity over and above amylase per se. condition to diagnose as failure to treat this appro-
It has been suggested, however, that the combination priately can lead to haemodynamic compromise due
of an elevated amylase and lipase level can imply sub- to an abdominal compartment syndrome and colonic
clinical pancreatitis. Contrast enhanced CT scanning perforation, which carries a 50% mortality rate. It is
can be used to confirm the diagnosis, and the manage- defined as massive acute colonic dilatation as a result
ment for the first couple of weeks is invariably organ of an imbalance in the autonomic supply to the colon
supportive. Parenteral or nasojejunal nutrition should rather than a true mechanical blockage. The diagnosis
be commenced if nasogastric (NG) aspirates are high, is suggested upon the presence of increasing abdomi-
although NG feeding itself is not contraindicated in nal girth with a tense, tympanic abdomen together
this group. There is no evidence for the use of prophy- with the inability to pass faeces or flatus. Diagnostic
lactic antibiotics and these should be reserved for cases confirmation can be made with an abdominal radio-
of infected necrosis where sensitivities can be obtained graph; however, a CT scan provides greater infor-
by radiologically guided percutaneous aspiration. mation and rules out the small possibility of a true
Rarely, in cases of advanced necrotising pancreatitis, mechanical blockage being present (e.g. sigmoid or
surgical necrosectomy is required which should ideally caecal volvulus). Pseudo-obstruction is more likely
be performed via a minimally invasive approach, or via to occur in patients with electrolyte imbalances, in
an open transabdominal or retroperitoneal approach particular potassium and magnesium. Indeed some-
if not. Attention should be drawn during the course of times the condition can be adequately treated with
pancreatitis to development of acute haemodynamic restoration of homeostatic levels of these cations
instability as this can suggest a ruptured splenic artery alone. Should colonic diameter exceed 10 cm or if the
aneurysm secondary to the local inflammatory pro- patient (if awake) complains of right iliac fossa ten-
cess. A specialist HPB opinion should always be sought derness, then urgent intervention is required as the
in cases of acute pancreatitis in this patient group. possibility of imminent perforation exists. Generally,
endoscopic decompression with a colonoscope can
Acalculous Cholecystitis relieve the impending perforation and on occasion
In the general population acalculous cholecystitis is a flatus tube is left in situ to aid the ongoing decom-
relatively rare, presenting in the sick and diabetics. In pression. In the general population the parasympa-
patients following cardiac surgery it occurs at least as thomimetic neostigmine has been used in refractory
frequently as calculous cholecystitis. The aetiology of cases of pseudo-obstruction; however, the cardiac risk
acalculous cholecystitis in this group is not entirely profile of this drug suggests its use may be limited in
clear but associations have been drawn with reduced patients following cardiac surgery. Surgical interven-
gallbladder contraction and ischaemia. The disease is tion is only required in cases of perforation where
suggested by intra-abdominal sepsis in the presence colonic resection, abdominal washout and stoma
of abnormal liver function tests as well as right upper formation are generally required. A drainage caecos-
quadrant pain in the awake patient. Diagnosis is con- tomy tube, which can be placed radiologically, is only
firmed by ultrasound or CT scanning. Aggressive and used in very rare cases of repeated caecal dilatation
early treatment is essential to prevent deterioration in a patient where laparotomy is not possible or safe.
and should consist of resuscitation and broad spec-
trum antibiotics. The risk of gangrene and subsequent Solid Viscus Perforation
perforation is far higher in patients with acalculous
Gastro-oesophageal perforation is a recognised com-
compared to classical calculous cholecystitis and for
plication of TOE. Presentation is often insidious, diag-
those that fail to improve rapidly early surgical inter-
nosis delayed and outcomes poor. Detection requires
vention is recommended, with cholecystectomy for
a high index of suspicion particularly when there has
those fit enough and percutaneous cholecystostomy
been difficulty in passing the probe or blood noted on
for those more acutely unwell.
removal, and in those with known gastro-oesophageal
pathology, small stature, advancing age, chronic ster-
Pseudo-obstruction oid use or undetermined source of sepsis. Oesophageal
Pseudo-
obstruction or Ogilvie’s syndrome is not perforation may also occur following radiofrequency
common after cardiac surgery but is an important ablation for atrial fibrillation, and in this instance
15:01:56
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298
there may be a coexisting atrial-oesophageal fistula. rare intra-abdominal complication following cardiac
Once suspected, the patient should be made nil by surgery but again has a mortality rate that exceeds
mouth, commenced immediately on broad spectrum that seen in the general population. The condition is
antimicrobials, and should undergo prompt inves- suggested by the presence of intra-abdominal sepsis
tigation with fluoroscopy or CT. Treatment options and lower abdominal pain which, whilst commonly is
include medical, endoscopic and surgical approaches; located in the lower left quadrant, can also be felt in
early involvement of upper GI specialists is essential the suprapubic region or lower right quadrant (as a
but despite this mortality is high. result of the sigmoid colon sometimes having a long
Perforated peptic ulcers have become far less com- mesentery). Diagnosis is made by contrast enhanced
mon since the widespread use of prophylactic proton CT scanning. The treatment in uncomplicated cases
pump inhibitors. Nevertheless, the condition does still (non-perforated) is broad spectrum antibiotics and
occur and the diagnosis should be entertained in the clinical observation. Patients with pericolic collections
presence of an acute episode of intra-abdominal sepsis or abscesses can be treated with radiological drainage
accompanied by pain in the awake patient. The diag- in addition to antibiotics. However, for those with
nosis can be made by either an erect chest radiograph generalised peritonitis or a free perforation radiologi-
or a CT scan, with CT scan having the greatest sen- cally, surgical intervention is required. Historically,
sitivity. Even with CT scanning it can be difficult to this would involve a Hartmann’s procedure consist-
locate the anatomical source for the free air seen radio- ing of sigmoid colectomy with an end colostomy.
logically. Increasingly, in the elderly and unfit, these Contemporary approaches, whilst still mandating
perforations can be managed conservatively as the the use of Hartmann’s procedure for those cases of
omentum will often adhere and seal the perforation generalised faecal peritonitis, also now include pri-
without intervention. The decision on non-operative mary anastomosis ± defunctioning stoma or laparo-
versus operative management should only be made scopic wash-out and drain insertion for less advanced
in conjunction with a senior and experienced general cases. Any septic deterioration in a patient managed
surgeon. Operative options vary from simple omental conservatively or otherwise should suggest an intra-
patching to, in advanced cases, partial gastrectomy. In abdominal collection which can be diagnosed with a
virtually all cases, managed either conservatively or CT scan and managed with antibiotics ± radiological
operatively, nasogastric drainage, parenteral nutrition drainage for those >2 cm in size.
and broad spectrum antibiotics (including H. pylori
eradication) are essential. If there is any septic dete- Conclusion
rioration following conservative or operative manage- Although not common, intra-abdominal complica-
ment, then concern should exist that the repair/patch tions occur at an elevated frequency in patients fol-
has broken down or an intra-abdominal collection has lowing cardiac surgery and carry a mortality rate
developed. Repeat CT scanning is essential in this situ- out of keeping with the pathological process. The
ation to define the problem, and allow potential radio- diagnosis of these conditions is made ever the more
logical drainage of any collection complex as they commonly occur in the early postop-
erative course where clinical signs are unreliable due
Diverticulitis to anaesthesia/sedation. Any suggestion of the devel-
opment of an acute abdomen should immediately
Diverticular disease is very common in the elderly –
warrant early involvement of an experienced general
it is reported that over 60% of patients >70 years of
surgeon to guide appropriate investigations and man-
age have diverticulosis. Around 10–25% of those with
agement. Delayed diagnosis should be avoided at all
diverticular disease will, at some stage, suffer an epi-
costs as mortality and morbidity rates are particularly
sode of diverticulitis. Whilst the majority of cases
high in this unique population group.
of diverticular disease in the Western population
occur in the sigmoid colon, pan-colonic diverticular
disease can also present. The phenomenon of ‘right- Learning Points
sided diverticular disease’ where multiple diverticula • Intra-abdominal complications are uncommon
are seen in the caecum and ascending colon, is more post cardiac surgery but carry a very high
common in an Asian population. Diverticulitis is a mortality rate.
15:01:56
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• Many gastrointestinal complications are difficult gastrointestinal complications. European Journal of

to diagnose in the critical care environment and Cardio-Thoracic Surgery. 2003; 23: 170–174.
may present subtly. Nashef SA, Roques F, Michel P, et al. European system
• The GICS (gastrointestinal complication score) for cardiac operative risk evaluation (EuroSCORE).
is a useful predictive tool to identify at risk European Journal of Cardio-Thoracic Surgery. 1999;
16: 9–13.
patients.
• Failure to progress in high risk patients should Passage J, Joshi P, Mullany DV. Acute cholecystitis
complicating cardiac surgery: case series involving
raise the possibility of a significant intra-
more than 16,000 patients. Annals of Thoracic Surgery.
abdominal pathological process. 2007; 83: 1096–1101.
• Early involvement of an experienced general
Pfutzer RH, Kruis W. Management of diverticular disease.
surgeon is essential to prevent a poor outcome. Nature Reviews Gastroenterology & Hepatology. 2015;
12: 629–638.
Further Reading Rattner DW, Gu ZY, Vlahakes GJ, Warshaw AL.
Anastassiades CP, Baron TH, Wong Kee Song Hyperamylasemia after cardiac surgery. Incidence,
LM. Endoscopic clipping for the management significance, and management. Annals of Surgery. 1989;
of gastrointestinal bleeding. Nature Clinical 209: 279–283.
Practice Gastroenterology & Hepatology. 2008; Rodriguez R, Robich MP, Plate JF, Trooskin SZ, Sellke
5: 559–568. FW. Gastrointestinal complications following cardiac
Andersson B, Andersson R, Brandt J, et al. Gastrointestinal surgery: a comprehensive review. Journal of Cardiac
complications after cardiac surgery –improved Surgery. 2010; 25: 188–197.
risk stratification using a new scoring model. Sessions SC, Scoma RS, Sheikh FA, McGeehin WH,
Interactive Cardiovascular and Thoracic Surgery. 2010; Smink (Jr) RD. Acute acalculous cholecystitis
10: 366–370. following open heart surgery. American Surgeon.
British Society of Gastroenterology Endoscopy 1993; 59: 74–77.
Committee. Non-variceal upper gastrointestinal Toumpoulis IK, Anagnostopoulos CE, DeRose JJ, Swistel
haemorrhage: guidelines. Gut. 2002; 51(Suppl 4): DG. Does EuroSCORE predict length of stay and
1–6. specific postoperative complications after coronary
D’Ancona G, Baillot R, Poirier B, et al. Determinants of artery bypass grafting? International Journal of
gastrointestinal complications in cardiac surgery. Texas Cardiology. 2005; 105: 19–25.
Heart Institute Journal. 2003; 30: 280–285. UK Working Party on Acute Pancreatitis. UK guidelines
Filsoufi F, Rahmanian PB, Castillo JG, et al. Predictors and for the management of acute pancreatitis. Gut. 2005;
outcome of gastrointestinal complications in patients 54(Suppl 3): 1–9.
undergoing cardiac surgery. Annals of Surgery. 2007; Vennix S, Musters GD, Mulder IM, et al. Laparoscopic
246: 323–329. peritoneal lavage or sigmoidectomy for perforated
Fiore G, Brienza N, Cicala P, et al. Superior mesenteric diverticulitis with purulent peritonitis: a multicentre,
artery blood flow modifications during off-pump parallel-group, randomised, open-label trial. Lancet.
coronary surgery. Annals of Thoracic Surgery. 2006; 2015; 386: 1269–1277.
82: 62–67. Zacharias A, Schwann TA, Parenteau GL, et al.
Musleh GS, Patel NC, Grayson AD, et al. Off-pump Predictors of gastrointestinal complications in
coronary artery bypass surgery does not reduce cardiac surgery. Texas Heart Institute Journal. 2000;
27: 93–99.
MCQs
1. What is the commonest form of postoperative gastro- (c) Perforated peptic ulcer
intestinal complication? (d) Pancreatitis
(a) Diverticulitis (e) Gastrointestinal haemorrhage
(b) Mesenteric ischaemia
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300
2. How quickly does a patient have to be bleeding in 4. Which electrolyte is most important in the pathogen-
order for a CT angiogram to identify a bleeding esis of colonic pseudo-obstruction?
location? (a) Calcium
(a) ≥0.1 ml/minute (b) Sodium
(b) ≥0.3 ml/minute (c) Potassium
(c) ≥0.5 ml/minute (d) Phosphate
(d) ≥1 ml/minute (e) Chloride
(e) ≥5 ml/minute 5. In non-occlusive mesenteric ischaemia what is the
3. What is the most appropriate first line test in a patient most appropriate first line management?
suffering a massive rectal bleed? (a) Laparotomy
(a) CT angiogram (b) Angiogram and embolisation
(b) Oesphogo-gastro-duodenoscopy (OGD) (c) Resuscitation and restoration of cardiac output
(c) Colonoscopy (d) Tranexamic acid
(d) Red cell scan (e) Broad spectrum antibiotics
(e) MRI
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Cardiothoracic Trauma
Chapter
35 Alia Noorani and Ravi J De Silva
Background Clinical Assessment and Resuscitation

Trauma accounts for up to 720,000 annual admis- As is usual management for any trauma patient, the
sions, and over 6 million attendances to the emer- ABC (airway, breathing, circulation) are established,
gency department in the UK. Thoracic injuries directly although modification of the ABC may be required in
account for 20–25% of deaths due to trauma and con- order to diagnose the extent of the injury and resusci-
tribute to 25–50% of the remaining deaths. Figures tate the patient simultaneously.
from the USA suggest that there are over 17,000 deaths Any patient with a compromised airway should
per year, directly attributable to chest trauma. undergo endotracheal intubation; this may prove
Unsurprisingly, there has been a steady increase in challenging, particularly in those with suspected
the number of penetrating injuries presenting to hos- cervical spine injury, as their neck must be immobi-
pitals. Concurrently, however, there have also been lised. Immediate chest decompression for a tension
significant improvements in pre-hospital and perio- pneumothorax is indicated, without requiring a chest
perative care facilities, meaning that there are now radiograph, and a sucking chest wound requires cover
more opportunities to save patients who, previously, to allow adequate ventilation. Presence of a haemo-
would have been declared unsalvageable. thorax requires chest drainage. Control of ongoing
The earliest written description of thoracic inju- haemorrhage and volume resuscitation are essential
ries dates back to the Edwin Smith Surgical Papyrus to maintain an adequate circulation.
in 3000 BCE. Later, Galen reported attempts to treat On examination of the patient, it is essential to
gladiators with chest injuries and Labeza in 1635 note the exact location of the injury and, in the case of
reported surgical removal of an arrowhead from the a missile injury, the entry and exit points.
chest wall of a Native American. In 1814 Napoleon’s An entry wound below the nipples and inferior
military surgeon reported various injuries to the to the scapula should be considered to be a trajec-
subclavian vessels. Until the late nineteenth century tory for an injury breaching the abdominal cavity.
most agreed with the sayings of Boerhaave that ‘all Gunshot wounds can penetrate any region of the body
penetrating cardiac trauma is fatal’, until the German and in the absence of an exit point with a definitive
physician Rehn in 1896 performed the first successful entry point, a retained projectile has to be considered.
cardiorrhaphy for a right ventricular injury sustained Besides causing direct injury, this could also have the
during a fencing match. potential to embolise within the vasculature. Cardiac
injury should be considered if entry points are present
anywhere between the two midclavicular lines. The
Mechanisms of Cardiothoracic Trauma commonest chambers to be injured are the right ven-
Cardiothoracic trauma can be broadly divided into tricle and the left ventricle.
penetrating or blunt trauma (Table 35.1). Blunt
trauma encompasses crush injuries, acceleration and
deceleration, blast injuries and direct blunt trauma. Imaging
Penetrating injuries include gunshot wounds, stab- A chest radiograph may confirm the presence of a
bing and shrapnel injuries (Figures 35.1–35.3). Only haemothorax or pneumothorax or a chest wall injury
10–15% of patients with blunt trauma and 15–30% of such as fractured ribs and flail chest as well as dia-
those with penetrating trauma require surgery. phragmatic injuries. Echocardiography can provide a
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Table 35.1 Types of cardiothoracic trauma and subsequent

effects
Penetrating Laceration of heart, great vessels, intercostal
vessels, lung parenchyma, airways,
oesophagus, diaphragm
Blunt Cardiac/pulmonary contusion
Rib fractures with or without flail segments,
thoracic spine fractures
Crush Ruptured bronchus, ruptured oesophagus,
cardiac and pulmonary contusion
Deceleration Aortic disruption, major airway injury,
diaphragmatic rupture
Blast Disruption of any intrathoracic organ
quick means to assess for the presence of pericardial

fluid; however this is an operator dependent imaging
modality and clinical signs should override an appar-
ently negative scan. CT scanning provides definitive
and rapid imaging for more subtle injuries that can-
not be diagnosed by clinical examination or simpler
modalities alone. The clinical stability of the critically
injured patient is paramount and no imaging should
take priority over management.
Specific Injuries
Chest Wall
The function of the chest wall is twofold: firstly to
to provide structural and functional assistance with
respiration and secondly to provide a rigid structure
comprising muscles and bony skeleton to protect
the intrathoracic and upper abdominal organs from
external forces.
In general, the majority of injuries to the chest
wall can be managed conservatively, with effective
pain control, pulmonary physiotherapy and early Figure 35.1 Penetrating trauma. This 42 year old man was
mobilisation. Specific patterns of injuries and the age impaled by a camping chair when he fell 15 feet off his roof into
of the patient are important factors to consider, and the garden. The steel chair leg was seen to be sitting anterior to
the heart and had caused only minor injury to the left lower lobe.
may require specialist care. For example, multiple rib Note that the bent leg of the chair can be seen outside the chest
fractures in the elderly may require early fixation to wall. The arrow is pointing to the leg of the chair in the coloured
aid with respiratory mechanics and avoid prolonged photograph.
ventilator assistance. Early epidural analgesia should
be considered in those with multiple rib fractures
and certain trauma guidelines suggest that thoracic Surgical management of flail chest segments (defined
epidurals should be used in patients over the age of as at least two fractures per rib in two or more ribs,
65 years with four or more rib fractures which are therefore unable to contribute to lung
Injuries to the first and second ribs indicate a expansion) have been shown to have benefits, such as
high velocity injury with significant impact force, and reduced duration of mechanical ventilation and ICU
other associated injuries must be sought and treated. stay, as well as lower odds of pneumonia or death.
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Chapter 35: Cardiothoracic Trauma
Figure 35.3 Penetrating trauma. This 28 year old patient

was impaled by an industrial drill bit whilst working on a
construction site.
Table 35.2 Indications for immediate thoracotomy

Immediate drainage of over 1500 ml of blood on chest drain
insertion
Ongoing bleeding at a rate of 200 ml/hr
Massive air leak
Persistent haemothorax despite adequate chest drainage
procedure, is not without complications and should

Figure 35.2 Penetrating trauma. This 45 year old patient had a be undertaken by individuals with adequate training
nail gun fired accidentally into his chest. The CT scan demonstrates and experience.
penetration of the left atrium and a left haemothorax.
Lung lacerations can be minor, or major, resulting
in bisection of a lobe, although even if a thoracotomy
is required, the majority of injuries can be managed by
Lung Injuries simple stapling or over sewing. Major injuries requir-
Blunt trauma can lead to significant pulmonary contu- ing a pneumonectomy are rare (less than 3%).
sions, air leaks and haemothorax. Penetrating trauma
leads to contusions from direct trauma as well as the
dissipation of kinetic energy. In general, the manage- Tracheobronchial Injuries
ment for pulmonary contusions is chest tube inser- These injuries can frequently be immediately fatal due
tion, which itself although a commonly performed to loss of the airway. Autopsy reports indicate that over
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304
3% of all trauma deaths have associated tracheobron- • A trauma patient with cardiac arrest after arrival
chial injuries. For those patients surviving to make it into the emergency department.
to the hospital, early suspicion and recognition of signs • Penetrating cardiac injuries with a short transport
is key. These injuries can present with subcutaneous time and with witnessed physiological signs of
emphysema, pneumothorax, massive air leak once life such as a pupillary response, spontaneous
a chest tube is in situ and haemoptysis. Urgent man- ventilation, measurable blood pressure and a
agement of the unstable patient requires immediate palpable carotid pulse, extremity movement and
securing of the airway followed by diagnostic flexible electrical cardiac activity.
bronchoscopy. Surgical repair is the treatment of choice Victims of penetrating trauma usually fare better than
for major lacerations, and the technique of repair those of blunt trauma, and of the victims of penetrat-
should be tension free to allow for optimal healing. ing trauma, those with stab wounds fare better than
those with gunshot wounds. A generous anterior thor-
Cardiac Injuries acotomy or bilateral anterior thoracotomies (clam
shell) should be performed. Once the chest is entered,
Blunt cardiac injury occurs due to an anterior force
evidence of tamponade is sought and relieved, if pre-
compressing the chest. The most common mecha-
sent. Immediate indications for a thoracotomy in
nism is compression of the heart between the sternum
a case of penetrating injury with cardiac arrest are
and the thoracic spine, although deceleration causes
shown in Table 35.2.
injury when the heart strikes the sternum freely.
Cardiac contusions can lead to dysrhythmias, valvu-
lar disruptions, myocardial infarction, myocardial Aortic and Other Great Vessel Injury
rupture and tamponade. Clinical evaluation includes Up to 15% of all deaths due to road traffic accidents
an ECG and an echocardiogram. Common ECG are due to injury to the thoracic aorta. Many of these
findings are a sinus tachycardia or atrial fibrillation. deaths are as a result of complete aortic transection.
Echocardiography can help rule out valvular insuffi- The majority of thoracic great vessel injuries occur
ciency or tamponade. due to penetrating thoracic trauma and about 20% of
Penetrating cardiac injuries are a highly lethal patients subjected to blunt aortic injury survive long
entity but urgent diagnosis and appropriate treatment enough to reach hospital, and of these the injuries are
can save patients. As a general rule, any wounds in the usually to the descending aorta. Blunt aortic injury
‘cardiac box’ area bounded by the midclavicular lines is second to blunt head injury as the leading cause of
laterally, the clavicles superiorly and the costal margins death due to road traffic accidents.
inferiorly should raise the suspicion of cardiac injury. The descending aorta is a relatively fixed
Stab wounds fare better than gunshot wounds and structure compared to the mobile aortic arch.
outcomes for single chamber injuries are better than The majority of aortic injuries therefore affect
when two or more chambers are affected. Although the junction of the arch and descending aorta at
the clinical signs of tamponade (Beck’s triad) are pre- the site of the ligamentum arteriosum (isthmus).
sent in 30% of cases, they are easily missed in a busy Endovascular management of these is now routine
emergency department setting. in specialist hands, and this approach is supported
Immediate surgical intervention is recommended by meta-analysis data.
for penetrating injuries to the anterior chest in a clini- Traumatic transection or dissection in the ascend-
cally unstable patient who cannot wait for diagnostic ing aorta will require open surgical intervention
imaging. Occasionally an emergency room thora- although these patients frequently do not make it to
cotomy may have to be undertaken to salvage a dying the hospital alive.
patient. The American College of Surgeons guidelines In the case of a clinically stable patient, further
on emergency department thoracotomy include the diagnostic imaging can be carried out to guide defini-
following: tive treatment. A chest X-ray is a useful screening tool
• Precordial wound in a patient with an out of and the presence of a left sided pleural effusion, wid-
hospital cardiac arrest. ened mediastinum or tracheal deviation may provide
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Chapter 35: Cardiothoracic Trauma
clues, although a CT scan would confirm these find- herniation and subsequent ischaemia due to strangu-
ings and indicate the precise location of the injury. lation is a serious complication of left sided trauma
and requires urgent repair. Right sided injuries are
Oesophageal Injuries thought to be less dire as the liver acts as a barrier for
herniation of bowel.
The oesophagus is infrequently involved in blunt
or penetrating trauma due, in part, to its protected
location. Additionally, injuries affecting the oesoph- Further Reading
agus are frequently associated with other severe Altinok T, Can A. Management of tracheobronchial
injuries (great vessels), which are often fatal even injuries. Eurasian Journal of Medicine. 2014;
before the patient presents to hospital. The presence 46: 209–215.
of a major oesophageal injury, however, can have Bertelsen S, Howitz P. Injuries of the trachea and bronchi.
seriously detrimental effects on the patient, leading Thorax. 1972; 27: 188–194.
to mediastinitis, multiorgan failure and death. The Karmy-Jones R, Wood DE. Traumatic injury to the
stable patient can undergo additional investigations trachea and bronchus. Thoracic Surgery Clinics. 2007;
including a CT scan and fluoroscopy. Endoscopy 17: 35–46.
should be undertaken in those with unclear imag- Pang D, Hildebrand D, Bachoo P. Thoracic endovascular
ing results. repair (TEVAR) versus open surgery for blunt
The clinical management of these patients includes traumatic thoracic aortic injury. Cochrane Database of
haemodynamic stability followed usually by surgical Systematic Reviews. 2015; 9: CD006642.
repair. Injuries diagnosed early can be treated with Simon BJ, Cushman J, Barraco R, et al. Pain management
primary repair, whereas those over 12 hours old are guidelines for blunt thoracic trauma. Journal of
Trauma. 2005; 59: 1256–1267.
best managed by multiple chest drain insertion.
Slobogean GP, MacPherson CA, Sun T, Pelletier M-
E, Hameed SM. Surgical fixation vs nonoperative
Diaphragmatic Injury management of flail chest: a meta-analysis. Journal of
In general, blunt thoracoabdominal trauma leads to the American College of Surgeons. 2013; 216: 302–311.
larger defects in the acute setting and the defect from Working Group, Ad Hoc Subcommittee on Outcomes,
a penetrating injury may be quite small to begin with American College of Surgeons, Committee on Trauma.
but enlarges over time due to a pressure gradient Practice management guidelines for emergency
between the abdominal and chest cavities. Visceral department thoracotomy. Journal of the American
College of Surgeons. 2001; 193: 303–309.
MCQs
1. The management of the trauma patient begins with 3. Diaphragmatic injuries:
assessment of the: (a) Are often left sided
(a) Airway and cervical spine
(b) May result in herniation of abdominal contents
(b) Breathing into the thorax
(c) Circulation (c) May present with acute respiratory distress
(d) Fractures
(d) Often require repair via laparotomy
(e) Head injuries
2. The commonest cardiac chamber to be injured by pen-
4. The second leading cause of death from blunt trauma
etrating trauma is the:
after head injury is:
(a) Left atrium
(a) Oesophageal perforation
(b) Right atrium
(b) Aortic injury
(c) Left ventricle
(c) Cardiac arrthymias
(d) Right ventricle
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306
(d) Rib fractures (b) Tension pneumothorax

(e) Pelvic fractures (c) Hypotension with systolic blood pressure of
5. Indications for immediate thoracotomy in the trauma 120 mmHg
setting include: (d) Flail chest
(a) Immediate drainage of over 1500 ml of blood on (e) Blast injuries
chest drain insertion following penetrating injury
that has resulted in cardiac arrest
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The Bleeding Cardiac Surgical Patient

Chapter
36 Jerrold H Levy, Kamrouz Ghadimi and Ian J Welsby
Introduction The bleeding patient in cardiac intensive care is

also resource consuming. The patient often requires
Bleeding is the commonest complication following
more than one nurse to help with blood sampling,
cardiac surgery. The amount of blood loss is used to
requesting products, administering volume, operat-
stratify patients in groups and judge their need for
ing cell savers, controlling temperature and frequent
return to theatre, risks of postoperative complica-
observations. The medical staff are often by this par-
tions, and need for transfusion of blood products.
ticular patient’s bedside. When numerous discus-
However, what is important for each individual
sions on how this patient is best managed are added,
patient is their demographic parameters, premorbid
the effort consumption detracts resources from other
state, type of surgery and the risks of undertaking
patients in the unit at the same time. Ironically, the
repeat operation.
bleeding patient is not only in a perilous state them-
Some patients suffer massive blood loss and surgi-
selves, but also exposes other patients to detriment.
cal control may not be possible. These patients may
Therefore careful early assessment and early manage-
need to be transferred to the intensive care unit with
ment are essential for successful outcome.
their chest open and packed with swabs. During the
time spent in intensive care, the coagulation abnor-
malities can be largely corrected, providing better The Bleeding Patient
opportunities for haemostasis when returning to Following cardiac surgery, bleeding is one of the
theatre. major expected associated problems. Therapeutic
An important feature of the bleeding patients in approaches include both prevention and treatment,
intensive care is the haemodynamic manifestation. and provide a unique opportunity to use prophylac-
This presents two types of problems: exsanguination tic therapies including antifibrinolytics. In the bleed-
and compression of structures by a clot. The intravas- ing patient, standard therapeutic approaches include
cular blood volume lost needs merely to be replaced. blood product administration, multiple concomitant
However, the correct formula for which product and pharmacological agents, and the increasing use of
how much is difficult to determine for each patient. both purified and recombinant haemostatic factors.
Laboratory blood tests and algorithms for how this It has been suggested that approximately 5–7% of
should be done are described below. It is also impor- patients bleed greater than 2 l of what may be reflected
tant to remember that sometimes the bleeding is so by chest tube drainage within the first postoperative
fast that mechanical infuser devices and cell savers are 24 hours. When bleeding occurs, about 5% of patients
needed. The second haemodynamic problem, com- require surgical re-exploration for bleeding. When
pression of structures by a clot, is more challenging. cardiac surgical patients develop bleeding, this will
A small amount of clot or fluid may be present in all increase the length of stay and is associated with a
cardiac surgical patients. When the amount of clot or higher mortality.
fluid impedes filling of chambers or vessels, or causes Multiple factors contribute to the complex causes
a compression effect (tamponade, Figure 36.1), it has of bleeding in cardiac surgical patients. This includes
to be evacuated. Clinical examination, vital signs surgical site bleeding, the effects of anticoagulants,
monitoring and echocardiography are used to guide including heparin, on platelet activation, contact
decision making in these circumstances. activation, fibrinolytic and inflammatory pathway
15:04:49
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308
Art BP Mean 200 40

100
Heart Rate 150
35
CVP 50 100
50
0 30
Interval Chest Dr... 500
0
Urine Output 100
50
0
Ventilation Mode Vol Contr Vol Contr SIMV (P→ Spontar→ Spontar→ Spontar→ SIMV (P→ SIMV (P→ SIMV (P→ PS/CPAP
PEEP/CPAP/pLow(observed) 5 4.5 4 4.8 4.6 4 3.6
FiO2 (Set) 60 50 51 50 51 51 40
PaO2 16.37 16.85 16.1 14.21 13.77 11.25 14.93
SaO2 98.6 98.7 98.5 97.8 97.8 99.1 96.8 97.9
PaCO2 4.38 4.2 4.52 5.03 3.91 5.66 4.49 5.63
CVP 0 6 13 6 11 20 17 10 11 15 13
Art BP Mean 40 72 77 74 94 69 55 55 72 82 72
Urine Output (Interval) 0 0 100 55 50 35 0 0 30 45 90 60
Metabolic
'pH 7.4 7.4 7.4 7.4 7.4 7.2 7.4 7.3
H+ 38.9 38.1 41.8 44.5 44.1 66.3 42.9 51.9
HCO3 20.3 19.9 19.5 20.4 16 15.4 19 19.6
Base Excess –3.6 –3.7 –4.8 –4.6 –8.3 –12.1 –5.6 –6.7
Lactate - ABG 1.4 1.3 1.7 2.3 4.4 9.1 3.8 3.3
2 3 Chest Drain: 27:49

3 2
Drugs (per interval) Units
Vasoactives
2 4 4 2 5
Glyceryl Trinitrate (GTN)
Figure 36.1 Clinical Information System (CIS) illustration of reducing urine output, followed by reduction in blood pressure and increase
in CVP and blood loss. (A black and white version of this figure will appear in some formats. For the colour version, please refer to the plate
section.)
activation, dilutional changes, hypothermia, and be discussed later, the critical role for fibrinogen lev-
other factors. Patients often are also on routine anti- els continues to evolve, with most data suggesting the
coagulants and antiplatelet agents that include oral importance of normalising fibrinogen in a bleeding
anticoagulants (warfarin, dabigatran, rivaroxaban, patient. With critical bleeds, and longer turnover time
apixaban, edoxaban) and platelet inhibitors (P2Y12 in standard laboratory testing, point-of-care testing,
receptor inhibitors –clopidogrel, prasugrel or tica- including rotational thromboelastometry (ROTEM©,
grelor). Thus, bleeding and coagulopathy following Tem International, Munich, Germany), thromboelas-
cardiac surgery are due to multiple factors that can be tography (TEG©, Haemonetics, Inc., Braintree, MA,
highly problematic after cardiopulmonary bypass. USA) and/or platelet function testing, is important.
In the actively bleeding patient, testing for platelet
Transfusion Algorithms and Bleeding dysfunction is unreliable as most tests need a rela-
Developing a specific therapeutic plan, especially with tively normal platelet count and most of the platelet
the use of transfusion algorithms, has been shown to function testing may not work following dilutional
consistently reduce allogeneic blood administration. It changes and activation after cardiopulmonary bypass.
is important to realise that any laboratory testing that
prevents empirical blood product administration is
important as part of a multimodal approach to blood
Allogeneic Blood Product
conservation and reduction of allogeneic blood prod- Administration
uct use. Transfusion algorithms generally recommend In the haemorrhagic patient, and from lessons learned
the following: administration of fresh frozen plasma in traumatic coagulopathy, the use of crystalloid and/
(FFP) when bleeding is accompanied by a PT or a or colloid administration may be helpful as first line
PTT > 1.5 times normal value, platelet transfusions therapy. With massive haemorrhage or uncontrollable
for thrombocytopenia with a platelet count <50,000– bleeding, however, these compounds do not provide
100,000, or cryoprecipitate or fibrinogen concentrates appropriate platelets or coagulation factors. The use of
when fibrinogen levels are <200 mg/dl (2 g/l). As will massive transfusion protocols, derived from lessons
15:04:49
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Chapter 36: The Bleeding Cardiac Surgical Patient
learned in traumatic coagulopathy, should be consid- Details of the variety of blood products are dis-
ered and implemented during uncontrollable bleeding cussed in Chapter 13.
in cardiac surgical patients. This routinely includes, in
addition to red blood cells, FFP, platelets and cryo- Fibrinolysis and Cardiac Surgery
precipitate (or fibrinogen concentrates). In European Activation of the fibrinolytic system is an important
countries, factor concentrates (e.g., fibrinogen and mechanism of vascular homeostasis. Mechanistically,
prothrombin complex concentrates) are increasingly plasmin generation is the enzymatic serine protease
used to restore circulating levels of critical factors for responsible for fibrinolysis and is formed following
haemostasis, and have been the subject of recent stud- the conversion of plasminogen to plasmin. Plasmin
ies. In addition, in the patient with massive haemor- is an enzyme that cleaves multiple proteins, includ-
rhage, hypothermia and acidosis frequently occur, ing fibrin but also fibrinogen. Following cardiopul-
requiring maintenance of normothermia and addi- monary bypass and/or tissue injury that occurs with
tional correction of metabolic abnormalities. surgery or trauma, fibrinolysis is activated and repre-
Of all the blood product administration used sents an important cause of coagulopathy. In trauma,
clinically, data elucidating when platelet transfu- orthopaedic surgery, and most importantly cardiac
sion should be administered are not clear. This is in surgery, multiple studies report the role of antifibrino-
part due to the problem of measuring platelet func- lytic agent administration in order to decrease bleed-
tion after cardiopulmonary bypass. In the bleeding ing and the need for allogeneic transfusions. These
patient, because of dilutional thrombocytopenia synthetic antifibrinolytic agents include the lysine
and acquired platelet dysfunction, platelets are often analogues, epsilon aminocaproic acid (EACA) and
transfused, but again monitoring platelet dysfunction tranexamic acid (TXA) that interfere with the binding
is problematic in this setting. This is further compli- of plasminogen to fibrin, necessary for activating plas-
cated by extensive use of antiplatelet medications as min. Aprotinin, a broad spectrum protease inhibitor,
outlined above. Whole blood clotting tests, including is a direct plasmin inhibitor. The specific antifibrino-
ROTEM© and TEG©, have been used as a monitor lytic agents will be considered as follows.
of platelet–fibrinogen interaction based on maximal
clot firmness or clot strength. With that said, these
values are indirect correlates and are highly affected Lysine Analogues
by fibrinogen levels. Most of the data on platelet The two antifibrinolytic agents administered clinically
administration are from oncology patients and we include EACA and TXA. As previously mentioned,
still do not know the critical platelet mass for surgical EACA and TXA competitively inhibit plasminogen
patients. Thrombocytopenia may not always correlate conversion to the active enzymatic agent plasmin.
with abnormal bleeding. TXA can also inhibit plasmin but at higher plasma
In the patient with ongoing haemorrhage, a mas- levels. Most of the studies and efficacy data with the
sive transfusion coagulopathy can develop, which is lysine analogues are reported with TXA, but EACA
defined as 10 or more units of packed red blood cells continues to be extensively utilised in the USA. EACA
(PRBCs) transfused in a 24 hour period, although does not consistently reduce transfusion require-
most of this literature is from trauma patients and ret- ments or surgical re-exploration, but it is inexpensive
rospective evaluations. Laboratory testing often lags and tends to be frequently substituted for TXA in the
behind blood product administration during these USA. Although multiple studies, primarily meta-anal-
scenarios. As a result, transfusion protocols have yses of randomised controlled trials, have reported a
been developed using fixed doses of FFP, PRBCs and decrease in bleeding in cardiac surgical patients, there
platelets that are administered as a fixed 1:1:1 ratio. In are limited safety data about the use of antifibrinolytic
cardiac surgical patients, there are few data to deter- agents. Most dosing studies include EACA at ~20 to 30
mine whether these therapeutic approaches improve g per case, or TXA at doses that range from 2 to 25 g,
bleeding outcomes although it may be logical to adopt although most TXA dosing regimens involve 2 to 8 g
massive transfusion protocols. In trauma and battle- dosing.
field patients, however, fixed ratios have become the One issue with TXA is the potential increased risk
mainstay of therapy although much of these data are of seizures. The incidence of postoperative convulsive
from retrospective analyses of large databases. seizures in a German hospital increased from 1.3% to
15:04:49
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310
3.8% after cardiac surgery, a finding that was noted to be inactivates the acidic heparin molecule via a simple
temporally associated with high-dose TXA. They noted acid–base interaction. Interestingly, protamine does
24 patients who developed seizures postoperatively and not reverse low molecular weight heparin. Following
had received high doses of TXA that ranged from 61 to cardiac surgery, patients are routinely overdosed with
259 mg/kg. The mean age of the patients was ~70 years, protamine for heparin reversal because most fixed
and 21/24 had undergone valve surgery/open chamber dose regimens for reversal involve protamine admin-
procedures. Although the underlying mechanisms are istration based on initial or total heparin dose, and do
not fully elucidated, TXA enhances neuronal excita- not account for the pharmacokinetics and/or relatively
tion by antagonising inhibitory gamma-aminobutyric short half-life of approximately 1 hour. Excess prota-
acid (GABA) neurotransmission. Lecker showed that mine should be avoided when reversing heparin as it
TXA inhibits neural glycine receptors, while inhibition potentially contributes to coagulopathy. Protamine is
of the inhibiting neurotransmitter glycine is an estab- an inhibitor of serine proteases involved in clot forma-
lished cause of seizures. Viewing the similarities in the tion as well as platelets.
chemical structure of TXA, GABA and glycine, it is Studies suggest that maintaining ‘adequate’ hepa-
conceivable that an interaction of TXA with the recep- rin levels during cardiopulmonary bypass and reversal
tors of both inhibitory neurotransmitters contributes doses of protamine based on the circulating heparin
to the increase in clinical seizures observed when TXA levels significantly reduce postoperative bleeding and
is given. However, in view of the chemical structure of the need for transfusions. Part of this efficacy may be
EACA and its close similarity to GABA and glycine as related to the effects of excess protamine on coagula-
well, it is noteworthy that it has not been reported to tion factors and platelets. Protamine has been shown to
produce neurological side effects. prolong the activated clotting time and cause platelet
dysfunction. When protamine is administered using
Aprotinin specific assays that determine the circulating heparin
levels, and based on the exact amount of protamine
This is a bovine serin protease inhibitor, which inhibits
needed, more complete reversal occurs with the low-
complement and contact factor activation via kallikrein
est activated clotting time (ACT) values. Additional
and plasmin activation. The half-life is 5–10 hours. In
studies have also reported that lower protamine doses
2008 Managno reported increased incidence of renal
reduce bleeding and transfusion requirements.
failure, myocardial infarction and heart failure in recip-
Other important causes of bleeding after prota-
ients. This led to the BART trial in 2008, resulting in
mine reversal include heparin rebound. This usu-
revoking of the drug license when an excess mortality
ally occurs approximately 2–3 hours after the initial
was found, despite beneficial effects on blood loss and
protamine dose, typically after the patient has been
transfusion. These findings have been disputed and
transferred to the intensive care unit. Heparin levels
aprotinin is available on a named patient basis for low
during this rebound time period usually range from
risk cases. Aprotinin affects celite based tests such as
0.1 to 0.3 IU/ml. Protamine doses of 5–15 mg at the
some aPTT reagents and can suggest profound coagu-
time of rebound may be effective at reversing hepa-
lopathy when in actual fact the patient has no excessive
rin rebound, rather than the 50 mg dose normally
bleeding. Heparin monitoring is also affected.
contained in the small ampoule which is commonly
administered. Studies have evaluated the ROTEM©
Other Pharmacological Adjuncts to assay for determining the need for additional prota-
Bleeding mine administration and note that most patients may
not need additional protamine within 30 minutes of
Protamine initial administration. Moreover, the ACT is not a sen-
Protamine is a highly basic polypeptide with molecu- sitive indicator of low heparin concentrations and is
lar weight around 5000 Da that contains ~70% argi- impacted by platelet counts and fibrinogen levels.
nine residues. Protamine is isolated from salmon
sperm, and exists in nature as a histone, a basic nuclear
protein that binds to DNA to provide structural integ- Desmopressin
rity in the nucleus. Currently, it is the only reversal Desmopressin (DDAVP) is the V2 analogue of argi-
agent for unfractionated heparin. This basic protein nine vasopressin used to treat diabetes insipidus but
15:04:49
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Chapter 36: The Bleeding Cardiac Surgical Patient
also stimulates the release of von Willebrand factor received rFVIIa to be relatively low and similar to
(vWF) multimers from vascular endothelium. vWF that among patients who received placebo. However,
is a critical protein that facilitates platelet adherence most case reports giving rFVIIa as rescue therapy
to damaged vascular subendothelium by acting as a include patients who have impaired coagulation, have
protein bridge between platelet glycoprotein Ib recep- received multiple transfusions and are at a high risk
tors and subendothelial vascular basement membrane for adverse events. The complex role that transfusion
proteins. DDAVP will decrease bleeding times with therapy has in producing adverse outcomes is increas-
mild forms of both haemophilia A or von Willebrand ingly being noted in the literature. In a large and com-
disease. Beyond these indications and despite wide- prehensive cohort of persons in placebo-controlled
spread perioperative use, efficacy is limited. Surgical trials of rFVIIa, treatment with high doses of rFVIIa
patients who potentially benefit from use of DDAVP on an off-label basis significantly increased the risk
are not well established, despite its frequent admin- of arterial, but not venous, thromboembolic events,
istration. DDAVP is administered intravenously at especially among the elderly.
doses of 0.3 μg/kg, and should be infused over 15–30 In the most recent cardiac surgical study, patients
minutes to avoid aberrancies in blood pressure or car- bleeding postoperatively >200 ml/hour were ran-
diac chronotropy. Most studies have not demonstrated domised to placebo (n = 68), 40 μg/kg rFVIIa (n = 35) or
efficacy or usefulness in cardiac surgical patients. 80 μg/kg rFVIIa (n = 69). The primary end points were
Mannucci reported that, despite 18 trials of desmo- the number of patients suffering critical serious adverse
pressin in 1295 patients undergoing cardiac surgery, events. Secondary end points included rates of reop-
there was only a minimal reduction of perioperative eration, blood loss and transfusions. Although more
blood loss (median decrease, 115 ml). Furthermore, adverse events occurred in the rFVIIa groups, they did
vasopressin is often administered to cardiac surgical not reach statistical significance (placebo, 7%; 40 μg/kg,
patients, which also has V2-and V1-receptor medi- 14%; P = 0.25; 80 μg/kg, 12%; P = 0.43). However, after
ated effects, and the additional benefit of administer- randomisation, significantly fewer patients in the rFVIIa
ing DDAVP in these patients is not clear. group underwent a reoperation because of bleeding
(P = 0.03) or needed allogeneic transfusions (P = 0.01).
Recombinant Activated Factor VIIa (rF VIIa) Summary

Recombinant FVIIa is approved for treatment of
The potential for haemorrhage in cardiac surgical
bleeding episodes and perioperative management in
patients represents an ongoing concern for manage-
adults and children with haemophilia A or B with
ment. Anticoagulation monitoring using point- of-
inhibitors, congenital factor VII deficiency, and
care testing, optimal use of transfusional therapies
Glanzmann’s thrombasthenia with refractoriness to
and adjunct administration of antifibrinolytics, as
platelet transfusions, with or without antibodies to
well as purified and recombinant therapies, provide
platelets; and for treatment of bleeding episodes and
clinicians with the ability to administer key coagula-
perioperative management in adults with acquired
tion proteins to treat haemorrhage. Although factor
haemophilia. However, it is also used off-label as a
concentrates represent an important potential thera-
prohaemostatic agent for life threatening haemor-
peutic approach to coagulopathy, other considera-
rhage. rFVIIa produces a prohaemostatic effect to
tions should include treating hypofibrinogenaemia,
mechanisms thought to be related to binding with tis-
thrombocytopenia and platelet disorders, or repairing
sue factor (TF) expressed at the site of vascular injury
surgical sources of bleeding. The integration of opti-
to locally produce thrombin and amplify haemostatic
mal use of pharmacological, transfusional and fac-
activation. The active form of FVII (FVIIa) accounts
tor concentrates into a comprehensive perioperative
for ~1% of circulating FVII, and has no effect until
coagulation treatment algorithm for bleeding is an
bound with TF. The therapeutic dose of rFVIIa in
important therapeutic approach for managing bleed-
non-haemophilia patients has not been established.
ing in cardiac surgical patients.
However, guidelines for off-label use are reported by
Goodnough and Despotis for life threatening haem-
orrhage. Controlled clinical trials report the incidence Learning Points
of thrombotic complications among patients who • Bleeding after cardiac surgery is multifactorial.
15:04:49
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• Antifibrinolytic agents are an important part of complications. Critical Care Medicine. 2006;
management. 34: 2729–2737.
• Transfusion algorithms are important for Koster A, Faraoni D, Levy JH. Antifibrinolytic therapy
reducing blood product administration and for cardiac surgery: an update. Anesthesiology. 2015;
bleeding. 123: 214–221.
• Fibrinogen is a critical component to target in the Levi M, Cromheecke ME, de Jonge E, et al.
bleeding patient. Pharmacological strategies to decrease excessive blood
loss in cardiac surgery: a meta-analysis of clinically
• Factor concentrates are increasingly used as relevant endpoints. Lancet. 1999; 354: 1940–1947.
therapies in managing bleeding.
Mannucci PM, Levi M. Prevention and treatment of major
blood loss. New England Journal of Medicine. 2007;
Further Reading 356: 2301–2311.
Despotis GJ, Grishaber JE, Goodnough LT. The effect of Sniecinski RM, Chandler WL. Activation of the hemostatic
an intraoperative treatment algorithm on physicians’ system during cardiopulmonary bypass. Anesthesia &
transfusion practice in cardiac surgery. Transfusion. Analgesia. 2011; 113: 1319–1333.
1994; 34: 290–296. Steiner ME, Despotis GJ. Transfusion algorithms and how
Gill R, Herbertson M, Vuylsteke A, et al. Safety and efficacy they apply to blood conservation: the high-risk cardiac
of recombinant activated factor VII: a randomized surgical patient. Hematology/Oncology Clinics of North
placebo-controlled trial in the setting of bleeding after America. 2007; 21: 177–184.
cardiac surgery. Circulation. 2009; 120: 21–27. Whitlock R, Crowther MA, Ng HJ. Bleeding in cardiac
Hein OV, Birnbaum J, Wernecke KD, et al. Three-year surgery: its prevention and treatment –an evidence-
survival after four major post-cardiac operative based review. Critical Care Clinics. 2005; 21: 589–610.
MCQs
True or False (c) Is associated with a decrease in bleeding
1. Multiple factors contribute to bleeding in cardiac sur- (d) Promotes fibrinolysis
gical patients, including: (e) Is associated with occurrence of seizures
(a) Effects of antithrombolytics 4. Protamine:
(b) Hyperthermia (a) Is an acidic polypeptide
(c) Contact activation (b) Has a molecular weight around 5000 Da
(d) Inhibition of fibrinolytic pathway (c) Is isolated from salmon sperm
(e) Dilutional changes (d) Can cause coagulopathy
2. In the bleeding patient, therapeutic approaches (e) Is an effective reversal agent for low molecular
include administration of: weight heparin
(a) Altepase 5. Desmopressin (DDAVP) is:
(b) Protamine (a) An analogue of arginine vasopressin
(c) DDAVP (b) Inhibits V2 receptors
(d) Apixaban (c) Stimulates the release of von Willebrand
(e) Prothrombin complex concentrate factor (vWF)
3. Tranexamic acid: (d) Is administered subcutaneously at doses of
(a) Activates conversion of plasminogen to plasmin 0.3 μg/kg
(b) Is typically given in doses of greater than 200 g
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Section 6 Perioperative Care: The Patient Post Cardiac Surgery
Management after Coronary Artery

Chapter
37 Bypass Grafting Surgery

Sam Nashef and Paolo Bosco
Professor Kolesov performed the first beating-heart

left internal mammary artery to left anterior descend-
Haemodynamic Management
In the majority of low-risk patients, there is no need
ing coronary artery bypass graft in February 1964
for cardiovascular support and an adequate cardiac
in Leningrad, Russia, whilst Dr Favaloro performed
output can be obtained just with fluid management
the first saphenous vein coronary artery bypass graft
and rate control by means of temporary pacing wires.
(CABG) surgery in May 1967 at the Cleveland Clinic
in the USA. Until then, treating angina using surgery, CO = HR × SV.
and the feasibility of operating on the delicate and
small coronary arteries had been unimaginable. Fifty The stroke volume, SV, is determined by preload, con-
years later, several million CABG operations have tractility and afterload.
been performed worldwide and it remains the most If contractility and afterload are within the nor-
common operation performed by cardiac surgeons mal range, it is obvious that cardiac output can be
with excellent outcome and very low mortality. optimised with fluids (preload) or by simply increas-
ing the heart rate with temporary cardiac pacing.
Patient Population Determination of the optimal filling pressure is often
Isolated CABG operations represent about 50–60% empirical and can be estimated with the use of a fluid
of the cardiac surgery workload in the UK. As per- challenge and observing the haemodynamic response
cutaneous coronary intervention is now often offered (see Chapter 14).
early in the course of ischaemic heart disease, patients If adequate perfusion pressure cannot be main-
presenting for CABG are now older and sicker and tained with these simple, first line measures, con-
this trend is set to continue. In addition, people live tractility and afterload may need to be addressed
longer due to advances in treatment of chronic dis- pharmacologically. Before making the diagnosis of
eases, including hypertension, elevated lipids, diabe- impaired contractile cardiac function, it is important
tes and others. Despite this, mortality from CABG is to exclude tamponade (see Chapter 3). Impaired con-
at an all-time low of between 1 and 2% due to better tractility can be improved with either pharmacological
perioperative management. A low-risk patient with a or mechanical means. Dopamine and catecholamines
competently executed CABG operation should have a are often the first choice but phosphodiesterase inhib-
smooth and uneventful recovery, an ITU stay shorter itors may be beneficial in right ventricular dysfunc-
than 24 hours and an overall hospital stay of around tion and elevated pulmonary vascular resistance (see
5 days. In a high-risk patient, however, with multiple Chapter 15).
risk factors and comorbidities, or after a suboptimally The most commonly used mechanical support
performed CABG operation, the procedure may be device is the intra-aortic balloon pump (IABP) (see
followed by complications and longer postoperative Chapter 21) which, by simultaneously decreasing
hospitalisation. myocardial workload and improving coronary per-
The limited functional reserve of elderly patients, fusion, can immediately alleviate myocardial ischae-
the presence of chronic kidney disease, peripheral vas- mia and improve poor cardiac function. The routine
cular disease, COPD, diabetes and impaired cardiac use of IABP in routine CABG is not necessary, but in
function are but a few of the challenges which may be selected high-risk patients there is a significant advan-
faced in the management of this high-risk population. tage in survival provided by this device. This was
15:05:37
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Section 6: Perioperative Care: Post Cardiac Surgery
supported by several randomised trials and a recent >10 times 99% upper reference limit from a normal
meta-analysis. preoperative level; and new pathological Q-waves or
The use of inotropic drugs, vasoconstrictors and new left bundle branch block (LBBB) or imaging or
mechanical support in the postoperative manage- angiographic evidence of new occlusion of native ves-
ment of the CABG patient can be guided by clinical sels or grafts, new regional wall motion abnormality,
assessment. Features of low cardiac output include or loss of viable myocardium. In daily clinical prac-
hypotension, poor peripheral perfusion, falling urine tice in many centres, cardiac biomarkers are not rou-
output despite adequate preload and metabolic evi- tinely measured after CABG surgery. Therefore, in the
dence of impaired perfusion, such as acidosis. In a immediate postoperative period, when the patient is
CABG patient with low blood pressure and inad- fully sedated and intubated, the first sign of possible
equate perfusion, it can sometimes be difficult to dif- ongoing myocardial ischaemia or infarction may be
ferentiate between inadequate filling (preload), poor unexpected haemodynamic or rhythm instability. This
cardiac function (contractility) or low systemic vas- finding should lead to a thorough assessment of the
cular resistance (afterload). The cause may also be patient, which includes ECG for new abnormalities,
multifactorial. If there is doubt in interpreting clini- echocardiogram for new regional wall motion abnor-
cal and simple haemodynamic findings, more invasive malities and cardiac biomarkers. If it is then believed
haemodynamic monitoring using transoesophageal that myocardial ischaemia is a genuine possibility, a
echocardiography or a pulmonary artery catheter will low threshold for emergency angiography should be
directly provide information on the cardiac output adopted. If a technical problem such as acute graft
and on the state of preload and afterload of both the or native vessel occlusion is demonstrated, surgical
pulmonary and systemic circulations, thus helping revision and emergency re-grafting of the affected
tailor the therapy to the haemodynamic needs of the territory should be considered as it may save both
patient. Routine use of a pulmonary artery catheter is myocardium and life. Additional treatment options
controversial and is not supported by clear evidence. include an intra-aortic balloon pump, GTN infusion,
Nevertheless, it may play a role in high-risk patients, antiplatelet agents and beta-blockers.
but the risk of adverse events and the costs associ-
ated with it suggest that its use be restricted to those
patients in whom the aetiology of the haemodynamic
Acute Kidney Injury
instability cannot be identified by more simple meth- Acute kidney injury (AKI) is a common postoperative
ods and those who require multiple vasoactive agents complication of cardiac surgery and is associated with
and their fine titration. an increased risk of morbidity, mortality and length
of stay
Between 5% and 30% of patients undergoing
Myocardial Infarction CABG may suffer this complication in the postop-
Myocardial ischaemic event presenting soon after erative period. The use of serum creatinine rather
CABG surgery is a rare but troublesome finding that than urine output as main criterion for the diagno-
can be difficult to diagnose and to treat. Many fac- sis of postoperative AKI is appropriate in the cardiac
tors can contribute to myocardial injury during a surgery population, since manipulation of the urine
CABG operation, including surgical trauma due to output with diuretics makes this a less reliable indi-
manipulation and suturing, less than ideal myocardial cator of AKI. A limitation of defining AKI based on
protection, incomplete revascularisation, acute graft serum creatinine measurements is the delay in detect-
thrombosis and iatrogenic injury to the native vessels. ing the onset of injury. Optimisation of renal perfu-
Because of these confounding factors, the diagnosis sion, avoidance of hypovolaemia and avoidance of
of MI following CABG is not straightforward and nephrotoxins are the only options to prevent or miti-
uncertainties remain around the correct threshold for gate the effects of postoperative AKI. Pharmacological
biomarker elevation and the need for associated crite- interventions have been attempted with inconsistent
ria. According to the 2012 third universal definition results, and there are no drugs that have demonstrated
of myocardial infarction after CABG, at least two of a definitive renal protection.
the following criteria should be present for diagnosis: The widely used drug furosemide was found not
cardiac biomarkers (with troponins preferred) rise to be protective and to be potentially harmful, as the
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Chapter 37: Management after Coronary Artery Bypass Grafting
incidence of AKI was twice that of the dopamine or aspirin administration include a reduction in mor-
placebo group in a double-blind randomised con- tality, myocardial infarction, stroke, renal failure and
trolled trial. Similar negative results have been seen bowel ischaemia. The antithrombotic effect of aspi-
in other studies. rin is greatly potentiated when used in combination
with clopidogrel. The use of dual antiplatelet therapy
Other Postoperative Complications following CABG is still controversial and a clear
Arrhythmia: Postoperative arrhythmia is common in benefit in vein graft patency has not been clearly dem-
cardiac surgical patients. The commonest observed onstrated. In conclusion, the use of aspirin within 6
arrhythmia is atrial fibrillation. The precise reasons hours following CABG is strongly recommended and
for developing arrhythmias are not always clear, but supported by clinical evidence.
overall the prognosis is good as frequently these
recover and sinus rhythm is restored. It is important Learning Points
to exclude poor right ventricular perfusion as a cause • CABG is the most common operation performed
of malignant ventricular arrhythmias. Occlusion of by cardiac surgeons, with an overall mortality
right coronary graft needs be ruled out in such cases. between 1 and 2%.
The treatment of postoperative arrhythmia is no dif- • The risk profile of the patient population is
ferent from the treatment for other patients in the changing, multiple comorbidities and advanced
ICU, and is described in Chapter 10. age are now common features of the patient
referred for CABG.
Heart block: Temporary heart block is not a promi-
• Fluid challenges and different pacing
nent feature of the CABG patients, but can occur. It
strategies can significantly increase the cardiac
normally resolves in the first few days, but sometimes
output.
needs implantation of a pacemaker system.
• Haemodynamic instability in the early
Postoperative bleeding: Patients undergoing coro- postoperative period may represent the first sign
nary surgery often receive antiplatelet medication, of ongoing myocardial ischaemia.
which may have long lasting effects, and hence they • In the appropriate clinical setting, the use of
are at a higher risk of coagulopathy. Thus postopera- aspirin within 6 hours following CABG is
tive bleeding can be a problem. The management of strongly recommended.
this problem is discussed in detail in Chapter 36.
Haemothorax: CABG patients are at a higher risk than

Further Reading
Chaikhouni A. The magnificient century of cardiothoracic
other cardiac patients of bleeding in the left hemitho- surgery. Heart Views. 2010; 11(1): 31–37.
rax when the left internal mammary artery has been
Dunning J, Versteegh M, Fabbri A, et al. Guideline on
used. The ICU team needs to be vigilant for this com-
antiplatelet and anticoagulation management in
plication if haemodynamic instability is a problem or cardiac surgery. European Journal of Cardio-Thoracic
if there is a massive blood loss postoperatively. Surgery. 2008; 34: 73–92.
Gukop P, Gutman N, Bilkhu R, et al. Who might benefit
Prevention of Early and Late Graft from early aspirin after coronary artery surgery?
Occlusion Interactive Cardiovascular and Thoracic Surgery. 2014;
19: 505–511.
Several randomised controlled studies, including a
Lassnigg A, Donner E, Grubhofer G, et al. Lack of
meta-analysis, have shown a clear benefit of early renoprotective effects of dopamine and furosemide
administration of aspirin in the prevention of early during cardiac surgery. Journal of the American Society
and late vein graft occlusion. This beneficial effect of of Nephrology. 2000; 11: 97–104.
early aspirin declines after 24 hours and disappears Lombardi R, Ferreiro A, Servetto C. Renal function after
after 48 hours. In the appropriate clinical settings, cardiac surgery: adverse effect of furosemide. Renal
early administration of postoperative aspirin follow- Failure. 2003; 25: 775–786.
ing CABG is not associated with increased blood loss Mangano DT. Multicenter study of Perioperative Ischemia
or transfusion requirement. The advantages of early Research Group. Aspirin and mortality from coronary
15:05:37
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bypass surgery. New England Journal of Medicine. 2002; Thygesen K, Alpert JS, Jaffe AS, et al. Writing Group on
347: 1309–1317. behalf of the Joint ESC/ACCF/AHA/WHF Task Force
Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury for the Universal Definition of Myocardial Infarction.
Network: report of an initiative to improve outcomes Third universal definition of myocardial infarction.
in acute kidney injury. Critical Care. 2007; 11(2): R31. European Heart Journal. 2012; 33: 2551–2567.
Sandham JD, Hull RD, Brant RF, et al. A randomized, Zangrillo A, Pappalardo F, Dossi, et al. Preoperative intra-
controlled trial of the use of pulmonary-artery aortic balloon pump to reduce mortality in coronary
catheters in high-risk surgical patients. New England artery bypass graft: a meta-analysis of randomized
Journal of Medicine. 2003; 348: 5–14. controlled trials. Critical Care. 2015; 19: 10.
MCQs
1. One hour following a routine CABG operation the of 80 over 55, CVP of 16 and a heart rate of 100 bpm.
mean pressure of your patient is dropping below The urine output is low and peripheral perfusion is
60 mmHg. Looking at the monitor you notice a sinus poor. What is your first action?
rhythm of 50 bpm and a CVP of 12. The patient is (a) Start adrenaline
not bleeding, there is no suspicion of tamponade and
urine output is adequate. You want to increase the car- (b) Give fluids
diac output in order to prevent obvious complication (c) Request ECG and echocardiogram
due to hypoperfusion. What is your strategy?
(d) Insert an intra-aortic balloon
(a) Insert an intra-aortic balloon
(e) Start GTN infusion
(b) Start noradrenaline
4. Mr Stone underwent a CABG operation in the morn-
(c) Pace the atrium at 90 bpm ing. Now it is 2 pm and the nurse calls you for poor
(d) Start adrenaline urine output since his arrival in the unit. Blood pres-
sure is 130/70, heart rate 80, CVP 10. Haemoglobin is
(e) Pace the ventricle at 90 bpm 95, base excess is −2 and lactate 2.5. On examination
2. Your patient has just arrived in the unit. Mr Cabbage you notice cold peripheries, but Mr Stone is otherwise
has just received a total arterial revascularisation by unremarkable. What is your approach?
a very experienced surgeon. When the nurses looking (a) Start noradrenaline
after him roll him slightly in order to insert the sliding
sheet and reposition him in the bed, you notice a sud- (b) Start GTN
den drop of the blood pressure. The monitor shows a (c) Start a furosemide infusion
BP of 50/30 a heart rate of 100 and a CVP of 4. What is
(d) Give a fluid challenge
your first action?
(e) Wait and see
(a) Give a rapid bolus of fluid
5. You are asked to prescribe the standard medication to
(b) Pace the heart at 120 bpm
be administered in the first 24 hours following a rou-
(c) Call the cardiac arrest team tine CABG operation for Mrs Dark. Which of the fol-
(d) Give a bolus of metaraminol lowing should be included in the list?
(e) Call the surgeon (a) Sildenafil
3. Mr Bacon is a 66 year old man with diffuse coronary (b) Warfarin
disease. His LIMA was not used since the flow was (c) Vasopressin
considered poor, and he received a triple vein graft.
(d) Aspirin
The surgeon is not too happy about him since the
conduits and the targets were poor. The patient shows (e) Lorazepam
some haemodynamic instability with a blood pressure
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Intensive Care Unit Management

Chapter
38 Following Valve Surgery

Yasir Abu-Omar and Shakil Farid
The post cardiac valve surgical patients follow the Several important structures that are in close prox-
same general management principles as any other imity to the aortic valve may be damaged at the time
cardiac surgical patients. Adequate basic require- of surgery. These include the bundle of His, the ante-
ments such as oxygenation, ventilation management, rior leaflet of the mitral valve and the ostial origin of
optimal heart rate and cardiac output, coagulation the coronary arteries. The bundle of His runs beneath
management and early detection and management of the commissure between right coronary and non-cor-
pericardial tamponade, as well as pain management, onary cusps. A deep suture placed in this region may
are not different. However, patients undergoing result in injury with resultant complete heart block.
valve surgery tend to have higher risks of morbid- The anterior leaflet of the mitral valve is separated
ity and mortality. They may require more invasive from the aortic annulus by the aortomitral curtain in
monitoring, including with a pulmonary artery the region of the non-coronary cusp and left coronary
catheter, and infusion of vasoactive medication. cusps. Iatrogenic damage to the anterior leaflet of the
Early re-evaluation of post- intervention valvular mitral valve may result in mitral regurgitation. Lastly,
function by echocardiography is frequently needed. due to the close proximity of the coronary ostia to the
Electrophysiological interventions and pacing tech- aortic annulus, there is a risk of coronary ostial block-
niques are needed more often than for uncompli- ade or compromise and ensuing ischaemia. Accurate
cated coronary artery bypass graft surgery patients. suture placement and carefully securing the prosthesis
Sometimes, patients at a particularly high risk need in place should reduce the risks of paravalvular leak.
preoperative ICU admission for preoptimisation. In Intraoperative transoesophageal echocardiogram
this chapter we will discuss the salient features and is essential in all cases of valvular surgery, allow-
basic principles of preoperative and postoperative ing for early detection and immediate correction of
heart valve pathology challenges and management complications.
in the cardiac surgical ICU.
Physiological Considerations
Aortic Valve Surgery In aortic stenosis, there is pressure overload of the left
Aortic valve replacement is generally indicated in ventricle that results in concentric hypertrophy and
patients with symptomatic severe aortic stenosis and/ diastolic dysfunction. The stiff non-compliant ventri-
or regurgitation. cle is dependent on adequate preload and atrial con-
Options for aortic valve replacement include traction –the latter may contribute up to 30% of left
stented and stentless xenograft tissue valves, mechani- ventricular filling.
cal valves, homografts and, less commonly, pulmo- In chronic aortic regurgitation there is a volume
nary autografts. as well as pressure load to the left ventricle, result-
ing in dilatation and hypertrophy. In the acute set-
Anatomical Considerations ting of aortic regurgitation, such as in cases of aortic
The commonest cause for aortic stenosis in elderly regurgitation secondary to infective endocarditis or
patients is degenerative calcific disease, while in aortic dissection, the left ventricle may be normal
younger patients the commonest aetiology is congeni- in size. These patients often display marked haemo-
tal bicuspid aortic valve. dynamic compromise with a small ventricle that has
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not adapted to the large regurgitant volume during be treated. These patients do not normally need ICU
diastole. post-surgical admission. However, in case of com-
plications intraoperatively and postoperatively, these
Common ICU Problems patients can need intensive care. Common reasons for
ICU admissions are haemodynamic instability (brad-
Aortic Stenosis ycardia, arrhythmia, hypotension, hypertension), pul-
Arrhythmia: Atrial arrhythmia must be immediately monary oedema, renal failure and stroke. The support
treated with antiarrhythmic medications as the atrial for these patients follows the same principles as for
contraction contributes up to 30% of the ventricular surgical aortic valve patients.
filling. The threshold for synchronised cardioversion Aortic Regurgitation
to maintain atrioventricular synchrony should be low,
especially in patients with haemodynamic compromise. Hypovolaemia: In the setting of diastolic dysfunc-
tion that accompanies ventricular hypertrophy, large
Bradycardia: Postoperative bradycardia is treated fluid challenges often result in minimal change in fill-
with atrioventricular sequential pacing in order to ing pressures. Adequate preload is important in these
maximise the cardiac output. Transient or permanent patients for maintenance of an adequate cardiac output.
complete heart block may occur following aortic valve
Hypotension: Hypotension is not uncommon following
surgery due to oedema, haemorrhage, debridement
aortic valve replacement for regurgitation. The reasons
or damage to the atrioventricular bundle. If complete
can be multifactorial, and include post cardiopulmo-
heart block persists for more than 4–5 days then due
nary bypass vasodilatation, low cardiac output due to
consideration should be given to the placement of a
reduced contractility, pericardial collection or reduced
permanent pacemaker.
preload. Post cardiopulmonary bypass vasodilatation is
Hypotension: Adequate preload is essential for not uncommon and is readily treated with vasopressor
patients with aortic valve disease due to accompany- medication. However, it is important to establish that
ing diastolic dysfunction. Hypotension and hypovol- this is the reason for hypotension, and not reduced car-
aemia must be avoided as they could lead to a vicious diac output or pericardial collection. Therefore, use of
cycle of coronary hypoperfusion, reduced cardiac out- ultrasound imaging to rule out a pericardial collection
put and worsening hypotension. and cardiac output measurement is advisable.
Bradycardia and complete heart block should be
Hypertension: Hypertension tends to develop a few treated in a similar fashion as for aortic stenosis (see
hours following surgery secondary to the relief of left above).
ventricular outflow tract obstruction, often in the set-
ting of left ventricular hypertrophy. Severe hyperten- Mitral Valve Surgery
sion should be aggressively treated in order to protect Mitral valve surgery is generally indicated in patients
the surgical aortic suture lines and reduce myocardial with severe mitral stenosis not amenable to percu-
oxygen demand. taneous mitral balloon valvuloplasty and those with
severe symptomatic mitral regurgitation.
Stroke: Stroke may be caused by emboli in the pres- Mitral valvular pathology may arise due to dys-
ence of atheromatous aortic disease, particularly in function of the mitral annulus, leaflets, subvalvular
elderly patients and/or those with known history of apparatus as a result of ventricular dysfunction or a
cerebrovascular disease. Cerebral hypoperfusion may combination of some or all of these components.
also lead to cerebral ischaemic injury with or without
concomittent embolism in light of the high prevalence
of large and small vessel cerebral vascular disease. Anatomical Considerations
Rheumatic heart disease is the commonest cause
TAVI Patients in ICU: Novel technology of minimally of mitral stenosis, whereas degenerative disease is
invasive treatment for aortic valve stenosis by percuta- the commonest cause of mitral regurgitation. Other
neous valve implantation has allowed for patients with causes of mitral regurgitation include ischaemic heart
greater comorbidities and hence high surgical risk to disease, rheumatic disease and endocarditis.
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Chapter 38: Management Following Valve Surgery
Figure 38.1 Mitral valve and its relation to

Sinus node
Central fibrous body various structures. (A black and white version
Atrioventricular node of this figure will appear in some formats. For
the colour version, please refer to the plate
section.)
Coronary sinus
Aortic leaflet
Circumflex artery Mural leaflet

Dominant right coronary artery
The mitral valve is a complex structure that has an reversible or irreversible) and occasionally right heart
important role in the left ventricular geometry and dysfunction. Affected patients are prone to low cardiac
function. The subvalvular apparatus, which includes output postoperatively as a result of low end-diastolic
the chordae tendinea and papillary muscles, plays and end-systolic volumes. The onset of congestive
an important role in maintaining the integrity of the heart failure may coincide with the development of
mitral valve as well as the function of the left ventricle. atrial fibrillation. Postoperatively, stroke volume is
The anterior and posterior leaflets of the mitral valve largely dependent on the maintenance of adequate
are arbitrarily divided into A1, A2, A3 and P1, P2, P3 ventricular preload. The pathology of degenerative
regions, respectively. The circumflex artery runs in the disease of the mitral valve causing mitral regurgitation
atrioventricular groove near the posteromedial com- ranges from fibroelastic deficiency to Barlow’s dis-
missure and in close proximity to the medial half of ease. Barlow’s disease is characterised by pronounced
the posterior leaflet of the mitral valve. Injury or com- annular dilatation, bileaflet prolapse and the presence
pression to the circumflex artery results in inferobasal of thick, spongy leaflets due to excessive myxomatous
and lateral wall ischaemia (Figure 38.1). tissue proliferation. It may also be associated with
The coronary sinus is close to the anterolateral annular calcification. Fibroelastic deficiency is found
commissure and adjoining part of the posterior leaf- in older patients whereas Barlow valve with congeni-
let, while part of the anterior leaflet is close to the non- tally excessive valve tissue is seen in younger patients.
coronary cusp of the aortic valve. Care must be taken There may be prolongation or rupture of the chor-
when annular sutures are placed in these regions. dae giving rise to a flail or prolapsing leaflet. Chronic
Mitral annular calcification causes difficul- mitral regurgitation causes volume overload of the left
ties and challenges during mitral valve surgery. ventricle that leads to ventricular and atrial dilatation.
Overenthusiastic decalcification of the mitral annu- Mitral regurgitation leads to increased ventricular
lus may result in atrioventricular disruption, which preload as the regurgitate volume generated during
is associated with high mortality and morbidity. systole returns to the ventricle during diastole. There
Excessive removal of the subvalvular apparatus may is also reduced ventricular stress along with reduced
result in left ventricular rupture. afterload due to offloading of the ventricle. As the
ventricle accommodates to the excess volume by dila-
Physiological Considerations tation, there is minimal elevation of the pulmonary
Mitral stenosis is generally associated with a small left vascular resistance initially. Increased pulmonary vas-
ventricular cavity size. Advanced cases may be com- cular resistance occurs due to chronic volume over-
plicated by pulmonary hypertension (which may be load, ultimately leading to left ventricular failure.
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Acute ischaemic mitral regurgitation is most dysfunction and may require treatment with appro-
often due to annular dilation and malfunction of priate inotropes.
coaptation due to ventricular remodelling. However,
it can also be due to ruptured chordae or head of the Atrial fibrillation: Many patients undergoing mitral
papillary muscle following myocardial infarction. valve surgery have pre-existing paroxysmal or chronic
The posteromedial papillary muscle is most com- atrial fibrillation. The Maze procedure or pulmonary
monly involved as it is only supplied by the posterior vein isolation may be used as an adjunct to mitral
descending branch of the right coronary artery (or valve surgery in these patients. A left atrial diameter of
the circumflex artery in the case of a left dominant less than 5 cm and duration of atrial fibrillation of less
coronary circulation). The heart has little time to than 5 years is associated with greater success of the
adapt to the regurgitant mitral valve, which results in Maze procedure. The left atrial appendage may also
rapid rise of pulmonary pressure, pulmonary oedema be excised or obliterated in these patients to reduce
and development of cardiogenic shock. This is associ- the risk of stroke due to chronic atrial fibrillation
ated with high mortality. and embolisation of thrombus from the appendage.
Chronic ischaemic mitral regurgitation is gener- In addition, around 30–40% of patients develop new
ally a disease of the ventricle. Features include annular onset of atrial fibrillation following mitral valve sur-
dilatation and tethering of the papillary muscle and gery needing electrical or chemical cardioversion with
posterior leaflet due to ventricular remodelling fol- amiodarone therapy.
lowing ischaemia.
Tricuspid Valve
Common ICU Problems Tricuspid valve surgery is commonly indicated for
Ventilatory failure: This can occur in patients with moderate– severe functional tricuspid regurgitation
long standing mitral stenosis who have pulmo- due to left sided valvular heart disease or less com-
nary hypertension. It is important to avoid hypoxia monly pulmonary vascular disease. Tricuspid valve
and hypercarbia in the early postoperative period. surgery is also indicated for right heart failure refrac-
Therefore management of pulmonary congestion by tory to medical therapy or progressive dilatation of
reducing preload (diuresis, haemofiltration, vasodila- the right ventricle. Severe tricuspid regurgitation is
tation), pulmonary vasodilatation and mechanical not a benign process because of its effects on systemic
ventilator support is important. Where prolonged venous congestion, atrial rhythm and right ventricu-
mechanical ventilation of the lungs is needed, the lar function.
team need to judge the risks of ventilator associated The tricuspid valve has three leaflets: septal, ante-
pneumonia and other complications of mechanical rior and posterior. The septal leaflet abuts the fibrous
ventilation versus earlier extubation. skeleton of the heart, as a result of which it cannot
dilate.
Right ventricular dysfunction: Following surgery The anterior leaflet is the largest of all the leaflets.
for mitral stenosis, right ventricular dysfunction nor- The tricuspid valve has papillary muscle and chordal
mally improves over time. However, right ventricular attachments to the ventricular septum, unlike the
dysfunction can be problematic. A pathophysiologi- mitral valve. The atrioventricular node lies just poste-
cal approach to treatment is advisable. Optimising rior to the commissure between the anterior and sep-
preload, and maintaining adequate contractility, tal leaflets. Deeply placed sutures in the medial half of
along with reduction in right ventricular afterload the septal leaflet may result in atrioventricular block.
where possible, are the usual strategies. Medical treat- The right coronary artery lies in close proximity to the
ment with phosphodiesterase inhibitors, intra-aortic posterior leaflet. A deep suture placed in this region
balloon counterpulsation and right ventricular extra- may result in injury to the coronary artery or kinking
corporeal support (temporary right ventricular assist of the artery.
device, Impella) may be needed. Most cases of tricuspid valve dysfunction are
caused by failure of the coaptation of the leaflets due
Left ventricular dysfunction: Correction of val- to annular dilatation. Tricuspid valve replacement
vular regurgitation often unmasks left ventricular is only rarely indicated, as an annuloplasty ring is
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adequate to correct functional tricuspid insufficiency recognised as a risk factor for left ventricular outflow
in most cases. tract obstruction and residual mitral regurgitation
following mitral valve surgery. SAM results from the
‘Venturi effect’ pulling the mitral valve leaflets into
Valve Implant Considerations the left ventricular outflow tract (LVOT). This may
result in obstruction of the LVOT along with severe
Choice of Prosthesis mitral regurgitation due to displacement of the ante-
According to the American Heart Association Guidelines rior leaflet.
2014, bioprostheses are recommended for patients over Intraoperative echocardiogram is essential to iden-
the age of 70 years while mechanical prostheses are tify the risk of SAM and detection should this occur.
recommended below 60 years of age provided there Predisposing factors for systolic anterior motion
are no contraindications to anticoagulation. Between include the following:
60 and 70 years either prosthesis is reasonable. Patient
choice is essential in the decision making process. 1. Narrow aortomitral angle (<120° pre repair).
2. Distance of the ventricular septum to coaptation
point of the mitral leaflet <2.5 cm.
Postoperative Anticoagulation 3. Posterior leaflet height >1.5 cm.
Prosthetic heart valves are susceptible to thrombosis. 4. Basal septal diameter >1.5 cm.
For patients with mechanical mitral valves and those
with associated risk factors (i.e. atrial fibrillation, pre- When identified intraoperatively, initial measures
vious thromboembolism and hypercoagulable con- include maintenance of adequate preload and reduc-
dition) receiving mechanical aortic valves, aspirin tion of tachycardia. If these conservative measures
(75—100 mg once daily) as well as warfarin (with a fail then insertion of a larger annuloplasty ring or a
target INR of 3) should be commenced in the early sliding annuloplasty should be performed in order to
postoperative period and continued in the long term. reduce the height of the posterior leaflet.
Bridging anticoagulation with unfractionated heparin Postoperative management for prevention of sys-
should be considered if warfarin therapy is interrupted tolic anterior motion includes the following:
for any future cardiac or non-cardiac procedures. 1. Maintenance of adequate preload.
For mechanical aortic valves without risk factors, 2. Increase afterload by using alpha agonists.
warfarin therapy with a lower target INR (2.5) and long- 3. Reduce tachycardia by using beta adrenoreceptor
term aspirin (75—100 mg once daily) should be used. blockers.
Aspirin (75—100 mg once daily) and warfarin 4. Avoidance of inotropic agents.
therapy (target INR 2.5) is recommended for the first
3 months following mitral valve repair or replacement Combined valvular pathologies
with bioprostheses.
Different valvular pathologies can occur in combina-
tion. The combination of aortic regurgitation along
Special Considerations with mitral regurgitation carries high periopera-
Mitral valve tive morbidity and carries the worst prognosis if left
untreated. The combination of these two pathologies
Repair of the mitral valve is preferable to replacement. causes left ventricular enlargement, increasing vol-
If replacement is carried out, the subvalvular appa- ume overload and ultimately ventricular failure.
ratus (papillary muscle and chordae) should be pre-
served in order to maintain left ventricular function.
Mitral repair is associated with better short-term and Key Points
long-term survival and less incidence of thromboem- • Following valve procedures, maintenance of sinus
bolism when compared to replacement. rhythm is beneficial in order to optimise cardiac
output, as is careful optimisation of ventricular
Systolic anterior motion filling pressures.
Mitral valve repair is occasionally complicated by • Valve procedures can be complicated by heart
systolic anterior motion (SAM). SAM has long been block due to haemorrhage, oedema, suturing
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or aggressive debridement near the conductive

tissue.
Further Reading
Bojar RM. Manual of Perioperative Care in Adult Cardiac
• Degenerative disease is the commonest cause Surgery, 5th edition. Oxford: Wiley-Blackwell, 2011.
of mitral regurgitation. Localised ventricular
Loulmet DF, Yaffee DW, Ursomanno PA, et al. Systolic
infarct along with asymmetric ventricular anterior motion of the mitral valve: a 30-year
remodelling affecting the posterolateral perspective. Journal of Thoracic and Cardiovascular
ventricular wall causes ischaemic mitral Surgery. 2014; 148: 2787–2793.
regurgitation. Functional mitral regurgitation Mackay JH, Arrowsmith JE (Eds). Core Topics in Cardiac
is caused by a severely impaired and dilated left Anesthesia, 2nd edition. Cambridge: Cambridge
ventricle. University Press, 2012.
• Although mitral and aortic valve diseases Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/
are the commonest indications for heart valve ACC guideline for the management of patients with
surgery, the tricuspid valve can be a potential valvular heart disease: a report of the American
source of considerable morbidity and mortality. College of Cardiology/American Heart Association
Task Force on Practice Guidelines. Journal of Thoracic
Tricuspid valve disease commonly occurs
and Cardiovascular Surgery. 2014; 148: e1–e132.
secondary to left heart disease or pulmonary
vascular disease. Varghese R, Itagaki S, Anyanwu AC, et al. Predicting
systolic anterior motion after mitral valve
• The type of valve prosthesis used is dependent on reconstruction: using intraoperative transoesophageal
the patient age, valve preference, comorbidities, echocardiography to identify those at greatest risk.
valvular pathology and the contraindications to European Journal of Cardio-Thoracic Surgery. 2014;
the use of anticoagulants. 45: 132–138.
MCQs
1. A 28 year old female needs an aortic valve replacement 3. After coming off bypass following aortic valve replace-
for severe symptomatic aortic stenosis. She wants to ment for severe aortic stenosis, the patient has a mean
complete her family within the next few years. What arterial pressure of 50 mmHg, heart rate of 45 beats/
are the options for management? minute and a central venous pressure of 12 mmHg.
Atrial and ventricular wires had been inserted before
(a) Mechanical prosthesis
coming off bypass. In order to increase the heart
(b) Bioprosthesis rate what is the best pacemaker mode that should be
(c) Ross procedure selected in order to optimise cardiac output?
(d) (b) or (c) (a) VVI

(e) Medical treatment until she completes her family. (b) AOO
2. An 80 year old female underwent mitral valve repair (c) DOO

for severe mitral regurgitation. After coming off (d) DDD
bypass her parameters were as follows: mean arterial
(e) VOO
pressure 45 mmHg, heart rate 95 beats/minute, cen-
tral venous pressure 10 mmHg. TOE revealed systolic 4. What is the commonest cause of mitral stenosis?
anterior motion of the mitral valve. What should be
(a) Degenerative
the next appropriate step?
(a) Increase the heart rate to 110 beats/minute (b) Rheumatic
(b) Start inotrope (c) Endocarditis

(c) Fluid bolus (d) Congenital heart disease
(d) Start noradrenaline (e) Carcinoid
(e) Observe
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5. After coming off bypass following mitral valve replace- (b) Injury to the circumflex coronary artery
ment there are ST depressions in leads I, II, V5, V6
(c) Injury to the left anterior descending artery
and regional wall motion abnormalities in the lateral
wall on TOE. What is the possible cause of the wall (d) Air embolism of the coronary arteries
motion abnormalities?
(e) Inadequate cardioprotection
(a) Injury to the right coronary artery
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Pulmonary Endarterectomy Patients in

Chapter
39 Cardiothoracic Critical Care
Choo Yen Ng
Introduction patients with distal disease and extreme pulmonary

hypertension (PH).
Chronic thromboembolic pulmonary hyperten-
sion (CTEPH) arises from total or partial occlusion
of the pulmonary vascular bed from non-resolving Pathophysiology
thromboemboli. Although pulmonary embolism It is uncertain why some patients have unresolved
(PE) is one of the more common cardiovascular dis- emboli, but a variety of factors play a role, alone
eases, CTEPH remains an under-diagnosed condi- or in combination. Initially, thrombus resolution
tion. CTEPH is defined as precapillary pulmonary probably results from a combination of thrombus
hypertension with mean pulmonary artery pressure fragmentation and endogenous fibrinolysis. In the
(mPAP) of more than 25 mmHg, pulmonary capillary majority of patients this leads to complete clot reso-
wedge pressure (PCWP) of less than 15 mmHg and lution. Further resolution relies on clot organisation
pulmonary vascular resistance (PVR) of more than 2 and neovascularisation, during which the obstructed
Wood units. vessel becomes recanalised and vessel patency is par-
CTEPH is a relatively rare but important sequela tially restored.
of deep venous thrombosis (DVT) and PE, where in After the clot becomes wedged in the pulmonary
up to 4% of patients, the acute embolic material fails artery, one of two processes occurs:
to resolve. Given that DVT and PE is as common as
1. The organisation of the clot proceeds to
1/1000 population per year, the annual incidence of
canalisation, producing multiple small
CTEPH may be of the order of 8–40 cases/million
endothelialised channels separated by fibrous
population. However, because some patients diag-
septa (i.e. bands and webs).
nosed with chronic thromboembolic disease have no
2. Complete fibrous organisation of the fibrin clot
preceding history of acute embolism, the true inci-
without canalisation may result, leading to a solid
dence of this disorder could be much higher.
mass of dense fibrous connective tissue totally
The majority of DVT and acute PE are managed
obstructing the arterial lumen.
medically with anticoagulation. Cardiothoracic sur-
geons rarely become involved in management of The generation of PH in CTEPH is not just the result
acute PE, unless it is in a hospitalised patient who sur- of simple obstruction of the pulmonary arterial bed;
vives a massive embolism that causes life-threatening indeed, there is little rise in pulmonary artery pres-
acute right heart failure and shock. Conversely, the sure following a pneumonectomy. The increased pres-
majority of CTEPH cases are amenable to surgi- sure as a result of redirected pulmonary blood flow in
cal treatment by pulmonary endarterectomy (PEA). the unobstructed pulmonary vascular bed can create
PEA is the definitive, and in most cases the curative, an arteriopathy in the small precapillary blood ves-
treatment for CTEPH. The objective of the surgery is sels similar to that seen in idiopathic pulmonary arte-
the normalisation of pulmonary artery pressure with rial hypertension. Hence, the pathogenesis of chronic
resultant significant symptomatic and prognostic thromboembolic occlusion in CTEPH with resultant
benefit. Medical management is only palliative, and raised PVR is thought to be secondary to obstruction
lung transplantation has an inferior outcome com- by thromboemboli and remodelling of the previously
pared with PEA and is only relevant for very selected normal pulmonary vascular bed.
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Chapter 39: Pulmonary Endarterectomy Patients
Clinical Presentation and Diagnosis

Clinical Presentation
There are no symptoms specific for chronic throm-
boembolism. The most common symptom associ-
ated with thromboembolic pulmonary hypertension,
as with all other causes of pulmonary hypertension,
is exertional dyspnoea. This dyspnoea is out of pro-
portion to any abnormalities found on clinical exami-
nation. Syncope, or presyncope, is another common
symptom in severe pulmonary hypertension.
The physical signs of pulmonary hypertension are
the same no matter what the underlying pathophysiol-
ogy. Initially the jugular venous pulse is characterised
by a large ‘A’ wave. As the right heart fails, the ‘V’ wave
becomes predominant. The right ventricle is usually
palpable near the lower left sternal border. The second
heart sound is often narrowly split and varies normally
Figure 39.1 Right pulmonary angiography of a patient with
with respiration. In the later stages of the disease, signs CTEPH demonstrating a web in the trifurcation of the lower lobe
of right heart failure predominate with oedema and vessels with complete occlusion of two segments of the lower lobe
ascites. Tricuspid regurgitation can be severe, with a and both segments of the middle lobe.
pansystolic murmur and an enlarged pulsatile liver.
Distal vessels demonstrate the rapid tapering and
Diagnosis pruning characteristic of pulmonary hypertension.
High index of suspicion and awareness of the dis- Other modalities of imaging, including multislice CT
ease is crucial. The chest radiograph may be entirely pulmonary angiogram and magnetic resonance angi-
normal. Pulmonary function tests reveal minimal ography, are gaining acceptance and are now favoured
changes in lung volume and ventilation. Diffusion over conventional angiography in some centres.
capacity is often reduced and may be the only abnor- Right heart catheterisation is crucial for the diag-
mality on pulmonary function testing. Most patients nosis of pulmonary hypertension, defined as a mPAP
are hypoxic. Dead space ventilation is increased. >25 mmHg at rest. Right atrial pressure, right ven-
The ventilation-perfusion lung scan is the essential tricular end-diastolic pressure, pulmonary artery
test for establishing the diagnosis. An entirely normal pressure and mixed venous O2 saturation are meas-
lung scan excludes the diagnosis of both acute and ured directly. Cardiac output and PVR can then be
chronic thromboembolism. calculated. Coronary angiography and other cardiac
Transthoracic echocardiogram (TTE) is usually investigations are recommended for patients over 40–
the test that gives the first indication of the presence of 45 years being considered for surgery.
PH. Systolic pulmonary artery pressure is significantly
raised. Features that may be seen on TTE depend on Management – Medical Treatment
the chronicity and degree of right ventricular failure; The main treatment of CTEPH is surgical and all
raised right ventricular dimension, impaired right ven- patients with suspected CTEPH should be referred to
tricular function and right ventricular hypertrophy. an experienced unit able to perform PEA. Untreated,
Currently, pulmonary angiography is said to be the the prognosis of CTEPH is very poor with severe
gold standard imaging test for evaluation of operability debilitation and premature death from right heart
in CTEPH, but experience is essential for the proper failure. In historical case series, the mean survival is
interpretation of pulmonary angiograms. Organised 6.8 years, and when the mPAP of patients with throm-
thrombi appear as filling defects, webs or bands, or as boembolic disease reaches 50 mmHg or more, the
completely thrombosed vessels ‘missing’ (Figure 39.1). 3-year mortality is about 90%.
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Chronic anticoagulation represents the mainstay Surgery is more successful in patients with types 1 and
of the medical regimen. Anticoagulation is primar- 2 disease, with a greater reduction in PVR and low-
ily used to prevent future embolic episodes, but it est mortality. Surgery in patients with the more dis-
also serves to limit the development of thrombus in tal type 3 disease is more challenging with a smaller
regions of low flow within the pulmonary vascula- reduction in PVR and higher risk. Patients with pre-
ture. Historically, inferior vena caval filters were used dominant type 4 disease are considered ‘non-operable’
routinely to prevent recurrent embolisation but this is or to have ‘non-surgical’ disease.
now not recommended, as there are few data to sup-
port this indication. Patient Selection
Data from clinical drug trials in CTEPH are lim- Main indications for surgery are symptoms and prog-
ited. Specific disease targeted drug therapy is therefore nosis. A patient with CTEPH, in WHO Class II–IV
not licensed for CTEPH patients, but drugs used for with significant pulmonary hypertension (mPAP
the treatment of idiopathic pulmonary arterial hyper- more than 25 mmHg), stands to benefit from PEA.
tension such as Bosentan and Sildenafil are sometimes This must be weighed against the amount of ‘cleara-
used and may provide symptomatic improvement in ble’ disease based on imaging and correlated to the pul-
some patients. monary vascular resistance measured preoperatively.
Other patient comorbidities that will be significant
Pulmonary Endarterectomy in a prolonged cardiopulmonary bypass time such as
age, known cerebrovascular condition, renal impair-
Operative Principles ment and intrinsic lung parenchymal disease should
The basis of the operation is the removal of the also be considered.
obstruction of the pulmonary vascular bed by endar-
terectomy within the superficial media of the arterial Surgical Techniques
wall. Therefore, the reduction in the PVR after pulmo- The approach is via a median sternotomy with car-
nary endarterectomy is dependent on the burden of diopulmonary bypass (CPB). The patient is cooled
‘clearable’ disease as defined on preoperative imaging. systemically to 20 oC and right and left pulmonary
The correlation between the degree of ‘clearable’ dis- arteriotomies are performed within the pericardium.
ease in imaging studies and PVR is the main deter- Adequate visualisation for distal dissection necessi-
minant of operability. The absolute preoperative and tates reduction in bronchial arterial collateral return
resultant postoperative PVR are also the main fac- to the pulmonary arteries. This is achieved by periods
tors that determine outcome after endarterectomy. of complete deep hypothermic circulatory arrest for
Mortality following endarterectomy may be five-to up to 20 minutes at a time with an intervening period
ten-fold higher in patients with a preoperative PVR of 10 minutes of re-perfusion on CPB. A cast of the
> 1200 dyne s/cm5. Similarly, a postoperative residual inner layer of the pulmonary arterial tree is then dis-
PVR of > 500 dyne s/cm5 is a risk factor for in-hospital sected free (Figure 39.2).
mortality. After completion of the endarterectomies, the
Although preoperative imaging helps to determine patient is rewarmed slowly on full CPB. The proce-
operability, the true extent of the disease can only be dure time is long because of the time necessary to cool
determined intraoperatively and has been classified in and warm on bypass.
four types: The aim is to achieve an immediate fall in mean PA
Type 1: Central disease where major vessel clots pressure by approximately 50%, and reduction in PVR
(fresh and/or mature) are present. to approximately one third of the preoperative level in
Type 2: Lobar and segmental disease where the majority of patients.
thickened intima is present with webs in the lobar
and segmental branches. Critical Care Management
Type 3: Subsegmental disease where the disease
begins distally at the subsegmental branches. General Principles
Type 4: Distal disease where small vessel disease is Most of the general principles of postoperative cardiac
present and represents inoperable disease. surgical care apply, but these principles centre around
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Figure 39.2 Endarterectomy casts from both pulmonary arteries of the same patient in Figure 39.1, demonstrating long tapering ‘tails’
which is a hallmark of good clearance. (A black and white version of this figure will appear in some formats. For the colour version, please
the management of the left ventricle. The management which impacts on right ventricular performance
of patients following PEA involves these two principles: upon weaning from cardiopulmonary bypass.
• Careful management of the right ventricle; Pulmonary vascular resistance in the post- PEA
• Minimising the pulmonary vascular resistance. patient can be affected by the following:
Most patients with CTEPH have a normal functioning • Right ventricular function, hence inexplicably
left ventricle in the absence of coronary atherosclero- linked;
sis and ‘left-sided’ heart valvular disease. Therefore left • Hypoxia secondary to poor perfusion
ventricular cardiac output and ultimately end-organ matching, intrinsic lung parenchymal disease,
perfusion is usually dependent on the contractile fluid overload, lung sepsis and mechanical
reserve of the right ventricle and pulmonary vascular complications such as pneumothorax;
resistance in the post-PEA patients. • Vasoconstrictor agents such as noradrenaline;
The contractile reserve of the right ventricle in the • High peak airway pressures.
post-PEA patients depends on the following: Considering the above factors when receiving a
• The varying degree of right ventricular patient onto the Critical Care Area (CCA) following
impairment secondary to CTEPH in the PEA surgery will help plan for potential problems that
preoperative period; may be encountered during the postoperative period.
• The post-PEA pulmonary vascular resistance that
is dependent on the amount of disease cleared
during PEA with resultant fall in pulmonary
Monitoring
Patients returning from the operating room following
artery pressure. High PVR in the postoperative
PEA surgery should have the following monitoring:
period can be due to technical failure to clear
‘surgical’ disease and/or presence of type 4 distal • 3 lead ECG monitoring;
disease (inoperable): • Pulse oximetry;
• Prolonged cardiopulmonary bypass, prolonged • Invasive radial and femoral arterial pressure;
myocardial ischaemic time and inadequate right • Invasive central venous pressure;
ventricular myocardial protection during PEA • Invasive pulmonary artery pressure;
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• Peripheral oxygen saturation and respiratory rate; Most patients who have had a good surgical clear-
• Blood temperature and end-tidal CO2 ance during PEA surgery with resultant mPAP of less
measurement. than 25 mmHg and a low PVR, who are haemody-
The femoral arterial line, which is placed after induc- namically stable with satisfactory acid–base balance,
tion, is used in preference to the radial line due to should achieve these ventilator targets by the first
damping associated with cooling and rewarming dur- postoperative day. The sedation is then turned off and
ing surgery. It is used for the first 12 hours in CCA the patient is allowed to wake up and is extubated.
before being removed and arterial monitoring reverts In some cases, it may be necessary to extubate the
back to the radial line. patient onto a continuous positive airway pressure
The balloon at the tip of the pulmonary artery cath- (CPAP) mask, especially when the PaO2 is borderline
eter is disabled and never inflated. Pulmonary artery low or the patient is cerebrally agitated or obtunded,
wedge pressure is taken as a default at 10 mmHg to to avoid hypoxia and maintain normocapnoea.
allow comparison of pulmonary vascular resistance
over time. Cardiac output and other haemodynamic Drugs and Antibiotic Prophylaxis
measurements are taken at 4 hourly intervals during The specific aim is to achieve a negative daily fluid bal-
the first 24 hours. The pulmonary arterial catheter is ance and support the right ventricle. Mannitol (12.5 g,
usually removed 24 hours after the patient is extu- 6 hourly for 6 doses) and furosemide (40 mg, 6 hourly
bated, and providing there are no concerns regarding for 6 doses then decrease to 8 hourly on day 2 and 12
residual pulmonary hypertension. hourly on day 3) are used to keep these patients ‘dry’.
At Papworth Hospital NHS Foundation Trust, the
Ventilation standard inotropic support following PEA surgery is
Patients are connected to the ventilator in the operat- dopamine at 3–5 µg/kg/min until the patients are dis-
ing room before weaning of cardiopulmonary bypass. charged to the ward.
The patient is then transferred to the CCA with the Rarely, the patients develop systemic hypertension
same ventilator to ensure a continuous level of posi- during the first 24 hours due to a systemic vascular
tive end-expiratory pressure (PEEP). resistance that remains high and this is associated with
A chest radiograph is usually obtained within an low or borderline low cardiac indices. Most patients
hour of arrival in the CCA, to exclude the presence can tolerate this and do not require intervention
of pneumothorax and early signs of reperfusion lung unless the low cardiac output impacts on end-organ
injury (see below). perfusion such as renal function. Phosphodiesterase
The patient is nursed in a slight upright position of inhibitor such as Enoximone is sometimes used in this
at least 30° to reduce the preload on the right ventricle. situation.
Recommended ventilator settings on arrival to the In situations where residual pulmonary hyperten-
CCA are as follows: sion remains post PEA surgery, preoperative drugs
such as Bosentan and Sildenafil may be continued
• SIMV or SIMV PRVC mode;
in the postoperative period. In cases where residual
• Fraction inspired oxygen percentage
pulmonary hypertension is significant post PEA with
(FiO2) of 80%;
concomitant right ventricular impairment or failure,
• Tidal volume set at 10 ml/kg; ilioprost (nebulised) is frequently used as an adjunct
• Respiratory rate at 16/minute; (see residual PH and right ventricular failure below).
• PEEP of 6 cmH2O; The prophylactic antibiotic of choice is Tazocin,
• Pressure support of 12 cmH2O above PEEP level. which is a combination antibiotic containing
An aggressive ventilator weaning protocol is adopted extended-spectrum penicillin antibiotic piperacillin
with the aim of facilitating extubation by the first and β-lactamase inhibitor tazobactam. The combi-
postoperative day. The FiO2 is decreased by 10% every nation has activity against many Gram-positive and
second hour, as long as the PaO2 is above 12 kPa (or Gram-negative pathogens and Pseudomonas aerugi-
every hour if PaO2 is above 25 kPa). Once FiO2 of 40% nosa. This covers both the sternotomy wound and the
is reached, the PEEP is decreased at a rate of 1 cmH2O potential pathogens that the lung may be exposed to.
every hour down to a minimum of 2 cmH2O. Peak air- In patients who have penicillin allergy, vancomycin
way pressure should be less than 30 cmH2O. and aztreonam are used instead.
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Fluid Balance and Renal Support Therefore, the threshold to perform CT brain
scans in these patients who do not wake up appropri-
The patient’s haematocrit is maintained above 30%
ately should be low to avoid missing treatable causes
(haemoglobin above 100 g/l) and human albumin
of an altered neurological state. Otherwise, if the CT
solution (4%) is the colloid of choice. Crystalloid is
scans are inconclusive, the treatment is largely sup-
avoided at all times.
portive and patients usually recover with conservative
In patients who develop acute or acute-on-chronic
management.
kidney injury secondary to the effects of prolonged
cardiopulmonary bypass and surgery, maintaining
aggressive diuresis can be challenging. Furosemide Specific Complications
may be switched to an infusion. Haemofiltration is
often used to maintain acid–base balance and main- Reperfusion Lung Injury
tain negative balance, especially when the kidney Reperfusion injury is defined as new radiological
injury impacts on ventilatory weaning and haemody- opacity in the lungs within 72 hours of pulmonary
namic stability. endarterectomy with associated hypoxia. The clini-
cal manifestation is that of focal or diffuse pulmonary
Haematology and Anticoagulation oedema. The radiological opacity can be segmental
or unilateral and is thought to reflect the segmental
Dilutional and consumptive coagulopathy is not
area where surgical clearance was most effective with
uncommon after a prolonged cardiopulmonary bypass
resultant sudden increase in perfusion.
with low platelet counts and clotting factors. Unless
Reperfusion injury that directly adversely impacts
there is significant bleeding, transfusion of blood
the clinical course of the patient occurs in approxi-
products such as pooled platelets, fresh frozen plasma
mately 10% of patients. In its most dramatic form, it
and cryoprecipitate are to be avoided in the first 24–
occurs soon after operation (within a few hours) and
48 hours. Infusion of these products into a pulmonary
is associated with profound desaturation with rapidly
vasculature that is denuded of its intimal layer can
worsening PaO2:FiO2 ratio.
result in release of cytokines and formation of micro-
Early measures should be taken to minimise the
emboli, which result in a rise of the mPAP and PVR.
development of pulmonary oedema with diuresis,
Enoxaparin 40 mg once daily is usually started on
maintenance of the haematocrit levels, and the early use
the evening of the first postoperative day. If the patient
of peak end-expiratory pressure. Once the capillary leak
is extubated, warfarin is commenced on the second
has been established, treatment is supportive because
postoperative day. If warfarin cannot be instituted,
reperfusion pulmonary oedema will eventually resolve
heparin infusion is commenced. This is an impor-
if satisfactory haemodynamics and oxygenation can
tant part of PEA management as anticoagulation with
be maintained. Venovenous extracorporeal membrane
warfarin or another novel direct Xa inhibitor like
oxygenation (ECMO) is sometimes necessary to pro-
Rivaroxaban is the mainstay of CTEPH prevention
vide temporary support when failure of adequate oxy-
post PEA surgery.
genation impacts significantly on end-organ functions.
Cerebrovascular Residual Pulmonary Hypertension and
Prolonged cardiopulmonary bypass and periods of
deep hypothermic circulatory arrest may impact on Right Ventricular Failure
the neurological function especially in the elderly. In The decrease in PVR level usually results in an imme-
addition, elderly patients on long term warfarin have diate and sustained restoration of pulmonary artery
a very small but significant prevalence of chronic sub- pressure to normal levels. Therefore right ventricu-
dural haematomas. Combined with a coagulopathy in lar function improves and cardiac output is often
the immediate postoperative period, all these can con- increased. In patients with residual PH, the postop-
tribute to cerebral agitation or obtunded neurologi- erative course can be difficult and the risk of death
cal state when sedation is switched off. In addition, is increased. The general principles outlined above
tranexamic acid infusion (started during surgery to explain the link between PVR and right ventricular
prevent fibrinolysis) may give rise to small incidences performance and the various factors that can affect
of epileptic fits. the relationship with often deleterious consequences.
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Pulmonary vasodilators (iloprost) and inotropic review of 230 patients, we demonstrated a signifi-
support (enoximone and judicious use of vasocon- cant improvement in NYHA class following surgery
strictor) are used in an attempt to improve right ven- (Figure 39.4). Five-year survival is nearly 90% even in
tricular performance and reduce PVR. If the surgical patients over 70 years of age.
clearance has been adequate and it is thought there
may be some reversibility (myocardial recovery fol-
lowing surgery and recovery from superimposed
Learning Points
lung sepsis), venoarterial ECMO may allow time for CTEPH is one of the most prevalent and increas-
recovery. ingly recognised forms of pulmonary hypertension
We have used ECMO to support patients with (PH) and should be considered in all cases with
severe reperfusion lung injury and residual PH post unexplained PH.
PEA. Up to 2016, 33 patients have been supported • Patients with CTEPH should receive lifelong
with successful weaning in 70% and long-term sur- anticoagulation and be considered for treatment
vival in approximately 50%. The period of ECMO sup- with pulmonary endarterectomy.
port has ranged from 48 to 1480 hours. • Pulmonary endarterectomy is the treatment of
choice in selected cases and may be curative with
Pulmonary Haemorrhage normalisation of pulmonary artery pressures and
significant symptomatic and prognostic benefit.
This is a rare, dramatic and often fatal complication
• Critical care management of patients following
of PEA that happens in the operating room around
pulmonary endarterectomy involves careful
the time of cardiopulmonary bypass wean. The clini-
management of the right ventricle and
cal manifestation is profound haemorrhage into
minimising pulmonary vascular resistance.
the bronchial airways resulting in severe hypoxia. It
• Reperfusion injury and residual pulmonary
results from perforation of the pulmonary arterial
hypertension with or without right ventricular
wall during dissection of the endarterectomy cast.
failure are treatable in the most severe form
Single lung ventilation with isolation of the
with venovenous or venoarterial extracorporeal
offending side is usually futile and the only option is
membrane oxygenation (ECMO).
conversion from cardiopulmonary bypass to central
venoarterial ECMO and reversal of systemic hep-
arinisation. If central venoarterial ECMO results in
a viable patient, the patient is brought back to the
Further Reading
CCA and maintained on ECMO until haemorrhage Madani M, Auger WR, Pretorius V, et al. Pulmonary
endarterectomy: recent changes in a single institution’s
into the airway has stopped. Bronchial toilet is then
experience of more than 2,700 patients. Annals of
performed to clear the airway before any attempts to Thoracic Surgery. 2012; 94: 97–103.
wean from ECMO. Mortality from this complication
Mayer E, Jenkins DP, Lindner J, et al. Surgical management
is nearly 100%. and outcome of patients with chronic thromboembolic
pulmonary hypertension: results from an international
Outcomes prospective registry. Journal of Thoracic and
Cardiovascular Surgery. 2011; 141: 702–710.
Since the year 2000, Papworth Hospital has been the
sole commissioned centre for pulmonary endarterec- NHS Information Centre for Health and Social Care.
tomy in the UK and we have seen a steady increase in National Audit of Pulmonary Hypertension, 2nd
annual report, 2011. Available at: www.ic.nhs.uk
the number of operations and improvement in results
over the last 10 years (Figure 39.3). Simonneau G, Robbins IM, Beghetti M, et al. Updated
clinical classification of pulmonary hypertension.
Over 1350 patients have now been operated on at
Journal of the American College of Cardiology. 2009;
Papworth and the current in-hospital mortality is 3– 54(Suppl): S43–S54.
4%. In a recent cohort, the median age was 60 years
Thistlethwaite PA, Makato M, Madani MM, et al. Operative
(range 15–84) with concomitant surgery being carried classification of thromboembolic disease determines
out in 10% of the cases. outcome after pulmonary endarterectomy. Journal
All PEA patients in the UK are reviewed at of Thoracic and Cardiovascular Surgery. 2002;
3 months and 1 year after endarterectomy. In a recent 124: 1203–1211.
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180
Papworth PEA Activity & Mortality
160 154
151
143
140
140
128
120
100
84
81
80
66
66.7
60
60 56
43
40
40 34 38
28.6 36.4 35.3
22 25.6
25
20 14 19.7
12.5
6 4 7.9 5.4 3.3 3.7 3.6 1.6 2.3 2.6 3.3 3.4
0
1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014
Year
Activity % mortality
Figure 39.3 Number of PEA operations in the UK.
NYHA Class
Pre-op 3 months 12 months
0.5%
8.5%
12.4%
12.3%
24.9%
30.9%
40.7%
50.3%
62.7% 55.9%
p < 0.001 vs preop p < 0.001 vs 3 months
NYHA Class
1.0 2.0 3.0 4.0
Figure 39.4 NYHA class: preoperative, at 3 months and 12 months follow-up.
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MCQs
1. Chronic thromboembolic pulmonary hypertension (c) Eisenmenger ’s syndrome
(CTEPH) is a precapillary pulmonary hypertension (d) Chronic thromboembolic pulmonary hypertension
that can be defined by one of these criteria:
4. Management of post-PEA patients in cardiothoracic
(a) Pulmonary artery wedge pressure of more than critical care revolves around one of these principles:
20 mmHg
(a) Inotropic support for the left ventricle
(b) Central venous pressure of less than 10 mmHg
(b) Aggressive use of vasoconstrictors
(c) Mean pulmonary artery pressure of more than
25 mmHg (c) Prolonged ventilation
(d) Cardiac index of less than 2.0 l/min/m
2 (d) Management of the right ventricle and pulmonary
vascular resistance
2. Which one of these symptoms is the most common in
patients with CTEPH? 5. Which one of these complications is NOT seen in
post-PEA patients?
(a) Persistent cough
(a) Left to right shunt
(b) Exertional dyspnoea
(b) Reperfusion lung injury
(c) Paroxysmal nocturnal dyspnoea
(c) Residual pulmonary hypertension
(d) Exertional angina
(d) Massive lung haemorrhage
3. Pulmonary endarterectomy is the definitive treatment
for one of the following:
(a) Idiopathic pulmonary hypertension
(b) Pulmonary venous hypertension secondary to
mitral valvular disease
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Heart Transplantation
Chapter
40 Stephen J Pettit and Anna Kydd
Introduction contraindications to heart transplantation; common

problems that may preclude heart transplantation are
Heart transplantation remains the definitive treatment
listed in Table 40.1. Finally, the team must enable the
for advanced heart failure that is refractory to con-
patient to make an informed decision about whether
ventional medical and surgical therapy. Over 110,000
they wish to be placed on the waiting list for heart
heart transplants have been performed worldwide.
transplantation. Intensive care doctors are important
Survival is excellent with a median survival of 11 years
members of the multidisciplinary team. Problems
for all patients and 13 years for patients that survive the
with airway management, vascular access, ventila-
first year. The majority of patients return to a normal
tory support, nutritional support and psychological
quality of life. Heart transplantation is limited by sup-
difficulties may be predictable in certain patients.
ply of suitable donor hearts. For this reason, the wait-
Postoperative critical care planning should begin at
ing time for heart transplantation is long and many
the time of preoperative assessment.
patients deteriorate while waiting. Selected patients
receive mechanical circulatory support with implant-
able or paracorporeal ventricular assist devices as a Transfer from the Operating Room
bridge to heart transplantation. These patients pose a It is important to understand any problems that were
particular challenge when they come to heart trans- encountered in the operating room at the point of
plantation, but their outcomes need not be adversely admission to the critical care unit. An early indication
affected. of allograft function will be given by visual inspec-
The time of greatest risk for mortality after heart tion of the donor heart as cardiopulmonary bypass
transplantation is during the immediate postopera- is weaned, the amount of cardiovascular support
tive period when patients are on the critical care unit. required, invasive haemodynamic data (cardiac index,
It is important that cardiac surgeons, cardiologists pulmonary capillary wedge pressure and right atrial
and intensive care doctors share an awareness of the pressure) and blood tests including mixed venous
goals of treatment and common problems in order oxygen saturation and serum lactate. In the most
to deliver excellent outcomes. Greater institutional severe forms of primary graft dysfunction, patients
experience is associated with a lower incidence of may leave the operating room with venoarterial extra-
complications and higher survival after heart trans- corporeal membrane oxygenation (VA ECMO) sup-
plantation. This is vital for the success of a transplant port. The team in the critical care unit should receive
programme because outcomes are closely scrutinised the patient and ensure that they are in a satisfactory
by regulatory bodies. haemodynamic state. Any immediate surgical prob-
lems should be identified before the operating room
Preoperative Assessment team stand down.
Patients are assessed by a multidisciplinary team
before acceptance onto a waiting list for heart trans- Postoperative Care
plantation. Assessment serves several purposes. The Excellent long-term outcomes after heart transplan-
team must determine whether the patient is expected tation are dependent on excellent postoperative care
to derive symptomatic and prognostic benefit from in the critical care unit. Patients change rapidly in the
heart transplantation. The team must identify any immediate postoperative period. Close observation
15:30:11 333
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334
Table 40.1 Common absolute and relative contraindications Table 40.3 Common problems after heart transplantation
to heart transplantation
Right ventricular dysfunction
Absolute Relative Acute kidney injury
contraindications contraindications Bleeding into pericardial or pleural space
Transpulmonary pressure Advanced age Sinus node dysfunction or high grade AV block
gradient >15 mmHg
Atrial arrhythmias
Pulmonary vascular resistance Body mass index >32 or
>5 Wood units <17.5 Systemic inflammatory response syndrome
Irreversible renal dysfunction Recent pulmonary

embolism
Mechanical ventilation must be used with care.
Sepsis or active infection Smoking, alcohol or
Excessive tidal volume and positive end-expiratory
substance misuse
pressure (PEEP) should be avoided. Both increase
Microvascular complications of Severe mental health
diabetes disorder
right atrial pressure, worsen tricuspid regurgitation
and increase right ventricular work by increasing
Malignancy within 5 years
(except skin)
pulmonary vascular resistance. Hypoxia should not
be permitted because it will cause pulmonary vaso-
constriction, increase pulmonary vascular resistance
Table 40.2 Principles of care after heart transplantation and increase right ventricular work. Inhaled therapies
such as nitric oxide and iloprost may be used to reduce
Support allograft function
pulmonary vascular resistance in selected patients.
Allow recovery of end-organ function
Establish immunosuppression
Avoid infection
Cardiovascular
Sinus node dysfunction and atrioventricular (AV)
block are common after heart transplantation. All
patients should leave the operating room with tempo-
by all members of the multidisciplinary team is vital. rary epicardial pacing wires. It is important to ensure
Treatment will need to be continually adjusted on an that these are attached to a temporary pulse genera-
individual patient basis. The basic principles of care tor and that the pacing system is working correctly.
are outlined in Table 40.2. Sinus tachycardia should be expected in the dener-
A series of investigations are routinely performed vated heart. However, this is not always present in
to assess allograft function and look for common the immediate post transplant period. Demand pac-
problems. These include regular blood gas analy- ing in a dual chamber mode (DDD) with a lower rate
sis, daily venous blood tests, an electrocardiogram, limit of 90–100 beats per minute is routine. A rela-
chest radiography and transthoracic echocardiogra- tively high heart rate may improve cardiac output in a
phy. Additional investigations such as cross-sectional transplanted heart when the ability to augment stroke
imaging and therapeutic drug monitoring assays are volume is limited. Pacing threshold, sensing and
arranged if needed. Surveillance endomyocardial underlying rhythm should be assessed on a daily basis.
biopsy is usually performed on a weekly basis during Sinus rhythm and AV conduction typically return
the first month after heart transplantation, but this is within 1 to 3 weeks of transplantation but around 10%
generally deferred until the patient is discharged from of patients will require a permanent pacemaker.
the intensive care unit unless there is specific concern All patients require continuous invasive monitor-
about acute rejection. Common problems after heart ing of cardiovascular performance in the immediate
transplantation are summarised in Table 40.3. postoperative period. This is most commonly achieved
with a pulmonary artery catheter. It is helpful to estab-
Airway and Ventilation lish desirable haemodynamic ranges; an example is
All patients will be sedated and mechanically venti- provided in Table 40.4. Measurements outside the
lated via an endotracheal tube until they are ready for desirable range should prompt review and exclusion
extubation. Many sedative drugs cause vasodilatation of a surgical problem such as haemopericardium or
and drive use of potentially deleterious vasopressors. haemothorax. In the absence of a surgical problem,
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Chapter 40: Heart Transplantation
abnormal haemodynamics may represent a target for Use of inotropic or vasoactive medications in iso-
treatment. Abnormalities such as hypovolaemia may lation or combination after heart transplantation is
be easy to identify and treat. It is important to rec- common but there is no good evidence base to sup-
ognise that right ventricular dysfunction is common port the superiority of any particular regime. Agents
after heart transplantation and a leading cause of pri- should be selected according to individual patient
mary graft failure. Risk factors for right ventricular physiology and the desired effect. The expected effects
dysfunction include older donor age, longer ischaemic in a typical patient are outlined in Table 40.5. In gen-
time, low donor height/weight relative to recipient eral, the dose of inotropic or vasoactive medications
and high pulmonary vascular resistance in recipient. should be minimised and the medications should be
Right ventricular dysfunction is normally identified progressively weaned as recovery of allograft and end-
by a low cardiac index and rising right atrial pressure. organ function is seen. Intra-aortic balloon pump
Treatment of right ventricular dysfunction is complex (IABP) counterpulsation will increase coronary blood
and the principles are outlined in Figure 40.1. It is vital flow and reduce left atrial pressure, both of which may
that high right atrial pressure is not permitted because be helpful in right ventricular dysfunction.
this will lead to right ventricular distension and a Mechanical circulatory support may be required
downward spiral of right heart failure. when inotropic, vasopressor/vasodilator and intra-aortic
balloon pump support is insufficient to achieve desired
haemodynamic parameters. Percutaneous devices to
mechanically support the right ventricle are now avail-
Table 40.4 Desirable haemodynamic parameters after heart able but have not been widely used after heart transplan-
transplantation
tation. VA ECMO is thought to be the best treatment for
Haemodynamic parameter Desirable range severe primary graft failure. Central cannulation may
Mean arterial pressure 70–90 mmHg
be preferable to peripheral cannulation to allow longer
support duration, permit left ventricular venting and
Mean right atrial pressure 5–12 mmHg
reduce the risk of peripheral vascular complications.
Mean pulmonary capillary wedge 5–12 mmHg
pressure
Primary graft dysfunction may improve sufficiently for
VA ECMO to be weaned in up to 90% of patients within
Cardiac index >2
1 week. In the most severe cases, central VA ECMO may
Mixed venous oxygen saturation >70%
be used as a bridge to acute re-transplantation.
Right ventricular dysfunction
Reduce preload Reduce afterload Optimise rhythm Increase contractility Maintain coronary perfusion
Diuretic infusion Correct hypoxia Base rate 90–100 bpm Inotropic support Intra-aortic balloon pump
Reduce PEEP Reduce PEEP Optimise AV delay Vasopressor
CVVH Pulmonary vasodilator Treat arrhythmias
Intra-aortic balloon pump
Persistent right ventricular dysfunction
Mechanical circulatory support

Percutaneous right ventricular assist device
Veno-arterial extra-corporeal membrane oxygenation
Para-corporeal right ventricular assist device
Figure 40.1 Treatment of right ventricular dysfunction. CVVH continuous venovenous haemofiltration.
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Table 40.5 Expected effects of agents used for cardiovascular support after heart transplantation
Agent Contractility SVR PVR

Adrenaline Increased Increased Neutral
Noradrenaline Increased Increased Increased
Dopamine Increased Increased Neutral
Arginine vasopressin Neutral Increased Increased
Type 2 PDEi Increased Decreased Decreased
Hydralazine Neutral Decreased Neutral
Renal ideally be performed before treatment, but treatment

should not be delayed if it is not possible to perform
Most patients sustain acute kidney injury (AKI) at
endomyocardial biopsy in a timely fashion.
the time of transplantation and the risk is greater
There is no consensus on the optimal regime for
in patients with pre-existing renal dysfunction. It is
immunosuppression, and practice varies between
imperative to avoid high right atrial pressure in order
transplant centres. Immunosuppression will also
to avoid right ventricular distension and progres-
vary between patients for reasons including renal
sive right ventricular dysfunction. Patients require
dysfunction and haematological abnormalities.
multiple intravenous medications in the immedi-
Most patients are maintained on three immunosup-
ate post-transplant period and a high urine output
pressive agents during the first year after transplan-
is essential to maintain fluid balance. Most patients
tation and two immunosuppressive agents in the
are treated with loop diuretics to maintain neutral
longer term.
or negative fluid balance. Continuous venovenous
haemofiltration (CVVH) may be required if patients Corticosteroids
have significant AKI and either important electro- All patients receive intravenous corticosteroids at
lyte disturbances, acidosis or a positive fluid bal- the time of transplantation and these are continued
ance and high right atrial pressure. One should aim until gastrointestinal absorption recovers. Steroids are
to wean CVVH as soon as possible to avoid platelet started at high doses, equivalent to 1 mg/kg predni-
consumption within the circuit and vascular access solone per day, then slowly weaned to a maintenance
complications. Care must be taken to adjust doses of dose, equivalent to 0.2 mg/kg prednisolone per day.
antimicrobial therapy in patients with postoperative Further reductions in corticosteroid dose and discon-
renal dysfunction, and introduction of potentially tinuation are guided by surveillance endomyocardial
nephrotoxic immunosuppressive medications may be biopsy.
delayed until recovery of renal function.
Proliferation inhibitors
Immunosuppression All patients receive a proliferation inhibitor at the
All recipients receive immunosuppression from the time of transplantation and these are continued life-
time of transplantation to reduce the risk of rejection. long. The first choice agent is mycophenolate mofetil
Hyperacute antibody-mediated rejection is rare in the (MMF). A specific preparation is prescribed due to
modern era because of matching to avoid ABO or HLA differences in bioavailability. Patients will receive
incompatibility, but should be considered in the event intravenous MMF until gastrointestinal absorption
of very early primary graft dysfunction. Acute cellular recovers. Oral MMF should be taken with meals
rejection remains a major problem and is challenging to reduce the incidence of gastrointestinal adverse
to diagnose due to lack of specific clinical features. In effects. Azathioprine may be used if MMF is not tol-
general, there should be a low threshold for treatment erated. Leucopenia is a common adverse effect and
of suspected acute cellular rejection. Most centres use the full blood count must be regularly measured.
10 mg/kg of intravenous methylprednisolone, admin- Proliferation inhibitors should be reduced or stopped
istered on 3 consecutive days, for treatment of acute if there is significant leucopenia, particularly in the
cellular rejection. Endomyocardial biopsy should context of infection.
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Calcineurin inhibitors (CNI) Prophylactic antiviral therapy may be used according

Most patients are treated with ciclosporin or tacroli- to donor and recipient cytomegalovirus (CMV) status.
mus after heart transplantation. Tacrolimus has a more Intravenous ganciclovir is started at the time of trans-
favourable profile of adverse effects than ciclosporin, plantation and switched to oral valganciclovir when
but there is no difference in survival. CNI may be started possible. The optimal duration of CMV prophylaxis
at the time of transplantation or delayed until recovery is uncertain. Many centres discontinue valganciclovir
from AKI if an induction agent is used. Therapeutic drug after 3 to 6 months depending on donor and recipient
monitoring is required to achieve a balance between CMV status, then monitor for CMV reactivation or
efficacy and toxicity. The most common adverse effect de novo CMV infection. Other antiviral agents may
of CNI is renal dysfunction, due to renal arteriolar vaso- be used if there are specific concerns about infec-
constriction. Patients may receive sublingual tacrolimus tion such as hepatitis or human immunodeficiency
or intravenous ciclosporin if they are unable to absorb virus (HIV) in either donor or recipient. Nystatin is
medications from the gastrointestinal tract. used to prevent mucocutaneous Candida infection.
Additional antifungal prophylaxis with an azole or
Mammalian target of rapamicin (mTOR) an echinocandin may be used if there are specific risk
inhibitors factors for fungal infection in the recipient.
Sirolimus or everolimus may be used in place of CNI
or proliferation inhibitors after heart transplantation. Other Issues
The major benefit over CNI is a lower incidence of Many other issues must be addressed in the criti-
renal dysfunction. However, mTOR inhibitors have cal care unit that are not unique to heart transplan-
a less favourable profile of adverse effects than CNI. tation. These include management and removal of
Wound healing delay is a particular concern in the pleural, mediastinal and pericardial drains. Feeding
immediate post-transplant period. must be established as soon as possible and total par-
enteral nutrition may be required if the gastrointes-
Induction agents tinal tract cannot be accessed or is not functioning.
Induction agents may be used at the time of heart Physiotherapy is an important part of the recovery
transplantation. These are antibodies directed against process and should be commenced as soon as possi-
components of the cell- mediated immune response. ble. Careful and close communication with the fam-
Anti-human thymocyte globulin (ATG) and anti- ily is required. Psychological support is likely to be
human lymphocyte globulin (ALG) are polyclonal anti- required for both patient and family, particularly if
bodies. Muromonab is a monoclonal antibody directed there are early problems with allograft function.
against CD3, expressed on T lymphocytes. Basiliximab,
daclizumab and inolimomab are monoclonal anti-
bodies directed against the interleukin- 2 receptor.
Discharge from the Critical Care Unit
Alemtuzumab is a monoclonal antibody directed against Discharge from the critical care unit should occur
CD52, expressed on B and T lymphocytes, as well as when the patient has been successfully weaned from
macrophages, monocytes and natural killer cells. There support and both allograft and end-organ function
is no evidence any induction agent improves survival continue to recover. The receiving medical team need
but they may reduce the incidence of acute rejection and to know the date of transplantation, current cardio-
allow CNI to be withheld until resolution of AKI. vascular function including any ongoing requirement
for pacing, details of renal function including the
need for postoperative CVVH, and details of current
Antimicrobial Prophylaxis immunosuppression including any induction agents
Most centres administer prophylactic antibiotic ther- that have been administered.
apy at the time of heart transplantation, based on local
resistance patterns and recipient colonisation. In gen-
eral, prophylactic antibiotics are stopped if donor cul-
Learning Points
ture results are negative. Co-trimoxazole is commonly • The period of highest risk for mortality occurs
used as prophylaxis against Pneumocystis jirovecii early after heart transplantation while patients are
during the first year after heart transplantation. on the critical care unit.
15:30:11 337
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• All patients will have a degree of right ventricular Grimm JC, Kilic A, Shah AS, et al. The influence
dysfunction after heart transplantation and of institutional volume on the incidence of
require careful individualised cardiovascular complications and their effect on mortality after
heart transplantation. Journal of Heart and Lung
support.
Transplantation. 2015; 34: 1390–1397.
• High right atrial pressure must not be permitted
Kobashigawa J, Zuckermann A, Macdonald P, et al.
because this will lead to right ventricular Report from a consensus conference on primary
distension and a downward spiral of worsening graft dysfunction after cardiac transplantation.
right heart failure. Journal of Heart and Lung Transplantation. 2014;
• Corticosteroids and proliferation inhibitors 33: 327–340.
are started at the time of transplantation but Lahm T, McCaslin CA, Wozniak TC, et al. Medical and
introduction of calcineurin inhibitors may be surgical treatment of acute right ventricular failure.
delayed until renal recovery if an antibody is used Journal of the American College of Cardiology. 2010;
56: 1435–1446.
for induction of immunosuppression.
Lund LH, Edwards LB, Kucheryavaya AY, et al. The
• All patients require antimicrobial prophylaxis
Registry of the International Society for Heart
from the time of transplantation. and Lung Transplantation: Thirty-second Official
Adult Heart Transplantation Report-2015; Focus
theme: early graft failure. Journal of Heart and Lung
Further Reading Transplantation. 2015; 34: 1244–1254.
Banner NR, Bonser RS, Clark AL, et al. UK Schulze PC, Jiang J, Yang J, et al. Preoperative assessment
guidelines for referral and assessment of of high-risk candidates to predict survival after heart
adults for heart transplantation. Heart. 2011; transplantation. Circulation: Heart Failure. 2013;
97: 1520–1527. 6: 527–534.
Costanzo MR, Dipchand A, Starling R, et al. The Singh TP, Milliren CE, Almond CS, et al. Survival benefit
International Society of Heart and Lung from transplantation in patients listed for heart
Transplantation guidelines for the care of heart transplantation in the United States. Journal of the
transplant recipients. Journal of Heart and Lung American College of Cardiology. 2014; 63: 1169–1178.
Transplantation. 2010; 29: 914–956.
Tallaj JA, Pamboukian SV, George JF, et al. Have risk factors
Dhital KK, Iyer A, Connellan M, et al. Adult heart for mortality after heart transplantation changed over
transplantation with distant procurement and time? Insights from 19 years of Cardiac Transplant
ex-vivo preservation of donor hearts after circulatory Research Database study. Journal of Heart and Lung
death: a case series. Lancet. 2015; 385: 2585–2591. Transplantation. 2014; 33: 1304–1311.
MCQs
1. Which of the following factors is not a contraindica- (b) Increasing pulmonary vascular resistance may be
tion to heart transplantation? helpful in the treatment of RV dysfunction
(a) Transpulmonary pressure gradient of 12 mmHg (c) High right atrial pressure may lead to worsening
(b) Patient age 72 years RV dysfunction
(c) Complete resection of adenocarcinoma of colon 2 (d) Venoarterial ECMO is not a treatment option for
years ago patients with severe RV dysfunction
(d) Pulmonary vascular resistance of 6.5 Wood units (e) Pacing should be minimised in patients with
RV dysfunction by setting a lower rate limit of
(e) Left lower lobe pneumonia 50–60 bpm
2. Which of the following statements about RV dysfunc- 3. Regarding use of antibody induction agents in heart
tion after heart transplantation is true? transplantation, which of the following is false?
(a) Shorter ischaemic time is a risk factor for develop- (a) Antithymocyte globulin may be used for induction
ment of RV dysfunction of immunosuppression
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339
(b) Use of antibody induction agents may reduce (c) Co-trimoxazole is used as prophylaxis against
the incidence of early rejection after heart Pneumocystis jirovecii infection
transplantation (d) Entecavir is used as prophylaxis in selected indi-
(c) Basiliximab may be used for induction of viduals at risk of hepatitis B infection
immunosuppression (e) Penicillin V is used as prophylaxis against encapsu-
(d) Use of antibody induction agents allows calcineurin lated bacterial infection
inhibitor introduction to be delayed until recovery 5. Which of the following treatments is not used to
from acute kidney injury decrease pulmonary vascular resistance after heart
(e) Use of antibody induction agents improves survival transplantation?
after heart transplantation (a) Nebulised iloprost
4. Regarding use of antimicrobial prophylaxis after heart (b) Intravenous noradrenaline
transplantation, which of the following is false?
(c) Reduction of PEEP
(a) Valganciclovir is used as prophylaxis against
CMV infection for 3 to 6 months after heart (d) Inhaled nitric oxide
transplantation (e) Intravenous type II phosphodiesterase inhibitor
(b) Nystatin is used as prophylaxis against
mucocutaneous Candida infection
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Lung Transplantation
Chapter
41 JS Parmar
Introduction nephrotoxic drugs can all result in the loss of kidney

function in the early postoperative period and this is
Lung transplantation is currently the most effective
associated with poorer outcomes.
treatment in carefully selected patients with a variety
Lung transplant patients are probably at higher
of end-stage lung diseases. The major indications for
risk of developing the ICU related neuromyopathy
lung transplantation are chronic obstructive pulmo-
as a result of the requirement for high dose steroids
nary disease (COPD), cystic fibrosis (CF), pulmonary
as part of the immunosuppression protocol. This can
fibrosis (PF) and pulmonary hypertension (PH). Sadly
have a significant impact on the process of rehabilita-
there is a critical shortage of donor organs, which
tion, necessitating longer stays in the ICU. If severe, it
results in the need for careful selection of patients to
can impact on the respiratory muscles and diaphragm,
maximise the benefit of a scarce resource. This care-
which can lead to poor airway clearance and the need
ful selection includes an assessment of the patient’s
for a tracheostomy.
abilities to withstand the rigors of lung transplanta-
tion. This assessment has relied on clinical judge-
ment of the patient’s condition performed by the
Early Post Transplant
multidisciplinary team.
Although a successful therapy with both prog-
Primary Graft Dysfunction (PGD)
The transplant process from the declaration of death
nostic and quality of life benefit, it is not a risk free
in the donor, to organ harvesting, cold storage and
enterprise. Most large volume centres quote a 1-year
finally reperfusion in the recipient places a huge stress
survival of around 85% and 5-year survival of approx-
on the organ. All of these essential steps may create
imately 60% with a median survival of 6.8 years.
an inflammatory milieu that increases the possibility
Lung transplant patients will routinely require
of alveolar oedema. The absence of lymphatic drain-
support in the ICU in the immediate post transplant
age in transplanted lungs, the primary mechanism for
period but may also develop issues post transplant
clearing excess alveolar fluid, means that the lung is
necessitating ICU admission. These two require-
exquisitely sensitive to these fluid shifts.
ments are distinct clinical entities and are considered
Primary graft dysfunction (PGD) is the syndrome
separately.
complex that describes the early allograft dysfunction
(<72 hours) and is the largest cause of early mortal-
General ICU Issues ity. It is clinically manifest by progressive hypoxaemia
Lung transplant recipients are vulnerable to a num- associated with radiological infiltrates, and shares
ber of specific issues related to their disease and treat- many similarities with acute respiratory distress syn-
ment. However, if they become critically ill they are drome (ARDS) in non-transplanted lungs. The syn-
also vulnerable to the general range of problems that drome is graded according to the International Heart
are seen in critically ill patients. These include prob- and Lung consensus document (Table 41.1).
lems with dysfunction of any of the major organ sys- It is important to exclude other causes of early allo-
tems. Two that require specific mention are kidney graft dysfunction such as infection, volume overload,
and neuromuscular dysfunction. The entire trans- torsion of the lung or compromise of the pulmonary
plant process places a huge strain on the renal system. venous anastomosis, and acute rejection. In the major-
Surgery, transfusion of blood products and the use of ity of cases with grade 1 or 2 dysfunction, a relatively
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Chapter 41: Lung Transplantation
Table 41.1 International Heart and Lung Transplantation

consensus on primary graft dysfunction
Grade PaO2/FiO2 Radiographic infiltrates

consistent with pulmonary
oedema
0 >300 Absent
1 >300 Present
2 200–300 Present
3 <200 Present
benign course is followed. However, the presence of

persistent grade 3 PGD (>72 hours) is associated with a
poor prognosis with estimates of 1-year survival vary-
ing from 30 to 60% and reduced long-term survival. Figure 41.1 PGD grade 3 at 48 hours. The patient is very hypoxic
A number of potential risk factors have been identified despite being intubated and ventilated and is requiring ECMO
support. The X-ray demonstrates extensive bilateral infiltrates.
which include: recipients with PH, IPF, sarcoidosis or
donors with obesity, older age, smoking, high alco-
hol intake, and possibly the use of cardiopulmonary
bypass. Treatment of PGD is principally about careful
fluid balance with supportive measures for oxygenation
and haemodynamics. Aggressive diuresis and protec-
tive lung ventilation are the cornerstones of manage-
ment for milder grades. For PGD grade 3, in addition to
the above support, measures such as venovenous extra-
corporeal membrane oxygenation may be required
(Figures 41.1 and 41.2). Some experimental approaches
have included instillation of surfactant directly into the
lung. Other potential treatments that are being explored
include aspirin, statins, stem cells and aprotonin.
Infections
The second biggest cause of early mortality in lung
Figure 41.2 PGD grade 3 at 1 week. The patient remains
transplant recipients in the ICU after PGD grade 3 intubated and ventilated but with clearance of the alveolar oedema
is infection. The lung transplant recipient is particu- and without ECMO support.
larly vulnerable to infection as the allograft is open
to the atmosphere and a number of the usual defence
jirovecii (PCP) can be problematic it should be remem-
mechanisms are compromised. Foremost of these
bered that the most common infections in this group
are the impairment of mucociliary function, reduced
are the same as for other critically ill patients. This
cough, pain and compromise of the innate and adap-
high-risk profile is managed early post transplant with
tive immune responses by immunosuppression. In
prophylaxis with broad spectrum antibiotics, oral and
addition, the use of mechanical ventilation along with
nebulised antifungals and target antiviral agents.
the multiple invasive catheters required to manage the
patient are portals for entry for infection in an immu-
nosuppressed patient. This vulnerability extends Bacterial Infections
across the whole microbial constellation and means Cultures are taken from the donor at the time of har-
that susceptibility to bacterial, fungal and viral infec- vesting and the generic universal prophylactic anti-
tions is increased. Whilst opportunistic infections biotic regime is adjusted if these are positive. Many
with low virulence organisms such as Pneumocystitis recipients will have pre-existing respiratory infections
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that may have antibiotic resistances. This is particu-

larly an issue in CF patients who are often colonised
chronically with Pseudomonas aeuroginosa, which is
present in the upper airways and often recolonises the
new lungs. This is managed with a pre-existing agreed
antibiotic protocol and usually consists of at least two
anti-pseudomonal agents that are given for 2 weeks
post transplantation.
Viral Infections
The desired T- cell inhibitory effects of the post-
transplant immunosuppression increase the suscep-
tibility to and reduce the recipient’s capacity to deal
with viral infections. Cytomegalovirus (CMV) is the
commonest viral pathogen in lung transplant recipi-
ents and is associated with increased risk of chronic
rejection in patients who develop CMV pneumoni-
tis. The greatest risk is in CMV mismatched patients
who are CMV naive and receive a positive organ. Figure 41.3 Bronchoscopic appearance of a right bronchial
All CMV mismatched patients and positive patients anastomosis, demonstrating a severely ischaemic airway with
superadded Aspergillus infection. (A black and white version of this
receive prophylaxis with initially ganciclovir and sub- figure will appear in some formats. For the colour version, please
sequently valganciclovir. refer to the plate section.)
Fungal Infections
Fungal infections cause significant morbidity and
mortality in recipients post lung transplant. Lung
transplants are particularly vulnerable to Aspergillus
fumigatus infections of the airways. This can range
from anastomotic infections that can result in air-
way complications to Aspergillus trachea-bronchitis
(Figure 41.3). Fortunately, angioinvasive aspergillosis
is a rare complication. To combat this potential com-
plication, early post transplant most patients receive
antifungal prophylaxis. Practices vary according to
the risk profile of the centre. We employ both topi-
cal nebulised amphotericin and oral itraconazole until
there is airway healing (Figure 41.4).
Disease Specific Issues
COPD
Figure 41.4 Extensive left sided Aspergillus bronchopneumonia
COPD remains the most common indication for lung complicating chronic rejection in a lung transplant recipient.
transplantation in the UK. With the rapid develop-
ments occurring in all areas of medicine leading to increasingly relevant clinical concern. Increasing
increasingly complex and aged patients comes the understanding of the impact of frailty on outcomes
potential for these patients to be more frail. Although is emerging, suggesting that determination of frailty
not exclusively a feature of age, it is recognised that may help to guide the appropriateness of therapy in
a significant proportion of elderly patients will have individuals. Currently frailty is not formally quanti-
features of frailty and as such this is likely to be an fied in lung transplantation. A number of studies have
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highlighted its potential utility in determining out- risk. The right ventricle (RV) in these patients has
comes in potential recipients. Early studies have sug- accommodated to chronic strain and is used to high
gested that patients with frailty syndrome are more filling pressures. The principle of drying the lungs out
likely to develop complications and be removed from and keeping the right sided filling low often means
the waiting list prior to transplantation. that the RV function is severely compromised and
may need support with inotropes. These issues are the
Cystic Fibrosis main reason for increased early mortality and mor-
bidity. However, it is reassuring that once through this
CF patients have markedly altered pharmacodynam- difficult period patients do have good median and
ics with rapid processing of a number of classes of long-term survival.
medications. This is particularly evident in the early
postoperative period when the requirements for anal-
gesia may be very high. A delicate balance between
Drug Interactions
Immunosuppression targeted at T cells is the cor-
comfort and respiratory depression may be difficult
nerstone of maintaining an allograft healthy in a
to achieve, often necessitating the need for either an
recipient. Although there is a paucity of randomised
epidural or patient controlled analgesia. The need for
controlled studies in lung transplantation to guide
opiates can increase the inherent propensity for bowel
therapy, there is a wealth of clinical experience (over
blockages in some CF patients and can be a very dif-
30,000 transplants worldwide). Most transplant units
ficult perioperative issue, which can have a major
use triple therapy consisting of steroids, a cell cycle
impact on their outcomes.
inhibitor (mycophenolate or azathioprine) with a cal-
cineurin inhibitor ((CNI) cyclosporin or tacrolimus).
Idiopathic Pulmonary Fibrosis (IPF) CNIs are highly dependent on normal renal func-
Patients with IPF have fibrosis of the lungs which tion and processing by the cytochrome P450 system.
results in shrinkage of the lung volumes and a conse- Impairment in either of these systems can make ade-
quence of this is a stiff and relatively poorly compliant quately immunosuppressing a patient difficult, lead-
chest. Post transplant these patients often have small ing to either drug toxicities and infection from over
stiff chests that require time to accommodate to the immunosuppression or an increased risk of rejection
new lungs. This may require protracted ventilation from under immunosuppression. As a guiding prin-
and gentle weaning. ciple, drugs which can have significant impact on the
cytochrome P450 system, either by enzyme induction
or inhibition, should only be started if absolutely nec-
Pulmonary Hypertension (PH) essary and with the appropriate dose adjustment for
Patients with PH have the most difficult perioperative the immunosuppression (see Table 41.2).
course with the worst 30-day survival. The presence of Similarly, avoidance of medications that can
PH is an independent risk factor for PGD, in addition adversely affect renal function is advisable (i.e.
the preoperative anticoagulation and selective pulmo- NSAIDs).
nary vasodilators all add significantly to the bleeding
Table 41.2 Drug interactions
Interaction Increased level Decreased level Increased Increased

of CNI of CNI nephrotoxicity hyperkalaemia
Drug Amiodarone Carbamazepine Aminoglycosides ACE inhibitor
Clarithromycin Phenytoin Amphotericin Amiloride
Ciprofloxacin Rifampicin Foscarnet Spironolactone
Diltiazem NSAIDs
Erythromycin
Fluconazole
Itraconazole
Voriconazole
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Bridging with ECMO
Patients who required respiratory support with
mechanical ventilation whilst waiting for lung trans-
plantation have historically had poor outcomes, and
this has been regarded as a contraindication. The
increasing experience and technical developments
in the delivery of respiratory ECMO support (veno-
venous) has led to dramatic improvements in the
utility of this treatment. A number of published case
series have described the ability to bridge patients
to successful lung transplantation. Transplants from
ECMO are usually more complicated, have a poorer
1-year and 5-year survival, but do provide a possible
intervention to extend the opportunity of transplant.
In these patients, support with ECMO is time sensi-
tive and this means that these patients require organs
urgently. To support this, it is vital that organs are pri-
oritised to these recipients.
Figure 41.5 An unenhanced CT scan of a patient post lung
transplantation. The CT scan demonstrates failure of the lung to
Late Admissions to ICU (After 1 Year) empty as a result of gas trapping from airway obliteration.
Most patients post lung transplantation enjoy good
quality of life with little need for hospital inpatient
care. Occasionally, they may require admission to ICU precipitating cause and support in this situation may
post transplant for allograft related issues. The two be needed to allow adequate diagnosis. Often this may
most common reasons are acute rejection and severe require ventilation to facilitate either bronchoscopy or
infections in the context of chronic lung allograft dys- CT scanning (Figure 41.5).
function (CLAD).
Acute rejection is most common in the first year Mobilisation
post transplant. Approximately a third of patients have Lung transplant recipients are unique in that they
one episode in the first year. It usually presents with an need to start exercising the implanted organ imme-
increase in breathlessness associated with a decrease diately and expose it to air, which increases the risk
in exercise tolerance. These symptoms may be sup- of infections. Early mobilisation and physiotherapy
ported with a fall in lung function and non-specific can improve the physiological parameters of the new
infiltrates on X-ray. The gold standard for diagnosis organ and avoid sputum retention and atelectasis.
is a transbronchial biopsy, which has a sensitivity and Additionally, many patients are relatively malnour-
specificity of around 80%. Most patients will respond ished prior to surgery, and mobilisation and nutrition
to enhanced immunosuppression with pulsed meth- can help build their strength to improve mechanics of
ylprednisolone; however, occasionally this may fail respiration.
and these patients may require respiratory support to Pain control after surgery is therefore impor-
allow time for resolution of the rejection episode. tant, and analgesia needs to be carefully balanced.
CLAD is sadly a progressive unresponsive disease Depending on the surgical approach, patient tailored
which is the biggest cause of death in patients after analgesia should be used as soon as the sedation has
3 years post transplant. The disease is characterised by been stopped. In general, patients undergoing ster-
progressive scarring and obliteration of the airways. notomy have relatively little pain and intravenous
The pathology shows fibromyxoid scarring initially of morphine or simple analgesics may be sufficient to
the small airways. This results in a loss of respiratory facilitate physiotherapy and mobilisation. Anterior
function with increasing symptoms of breathlessness. mini- thoracotomies are also relatively favourable
In some patients with progressive allograft dysfunc- with regard to pain control. However, posterior thora-
tion, a significant infection may be the presenting or cotomies involving rib resections and extreme rib
15:32:38
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retraction, as well as clam-shell incisions, tend to be

more painful. Many of these patients need regional
Further Reading
anaesthesia in the form of nerve blocks or thoracic epi- Bulack BC, Hirji SA, Hartwig MG. Bridge to lung
transplantation and rescue post-transplant: the
durals. In general pre-emptive epidurals are avoided
expanding role of extracorporeal membrane
for two reasons: not all patients need them; there is oxygenation. Journal of Thoracic Disease. 2014;
a risk of intraoperative need for extracorporeal sup- 6: 1070–1079.
port or cardiopulmonary bypass involving systemic
Christie JD, Carby M, Bag R, et al. Report of the ISHLT
anticoagulation, hence a high risk of epidural haema- Working Group on Primary Lung Graft Dysfunction
toma and paraplegia. If needed, epidurals are usually part II: definition. A consensus statement of the
offered to selected patients postoperatively in the ICU. International Society for Heart and Lung
Good analgesia facilitates early mobilisation and Transplantation. Journal of Heart and Lung
physiotherapy, as well as lowering the risk of nausea Transplantation. 2005; 24: 1454–1459.
and gastrointestinal failure. The lower risk of gastroin- Christie JD, Edwards LB, Kucheryavaya AY, et al.
testinal failure allows for early nutrition and recovery. International Society of Heart and Lung
Transplantation. The Registry of the International
Conclusions Society for Heart and Lung Transplantation: 29th adult
lung and heart-lung transplant report – 2012.
Lung transplant recipients are an extremely vulnera- Journal of Heart and Lung Transplantation. 2012;
ble cohort of patients, who require careful attention to 31: 1073–1086.
detail to ensure that they gain the best outcome from Issa N, Kukla A, Ibrahim HN. Calcineurin inhibitor
their treatment. The combination of sick recipients nephrotoxicity: a review and perspective of the
with complex and involved surgery, immunosuppres- evidence. American Journal of Nephrology. 2013;
sion and the heightened risk of infection adds com- 37: 602–612.
plexity to their management. Javidfar J, Bacchetta M. Bridge to lung transplantation
Although transplantation is not a risk free enter- with extracorporeal membrane oxygenation support.
prise and in lung transplantation the risks are high, Current Opinion in Organ Transplantation. 2012;
it is also a highly rewarding endeavour offering the 17: 496–502.
patients both prognostic benefit and improvement in Kotloff RM, Thabut G. Lung transplantation. American
quality of life. Journal of Respiratory and Critical Care Medicine. 2011;
184: 159–171.
Learning Points Malagon I, Greenhalgh D. Extracorporeal

membrane oxygenation as an alternative to
• Lung transplantation is limited by shortage ventilation. Current Opinion in Anaesthesiology. 2013;
of donor organs. The hospital mortality is 26: 47–52.
approximately 10%. Shah RJ, Diamond JM, Cantu E, et al. Objective
• Early complications such as rejection and estimates improve risk stratification for primary
infections can be successfully treated in most graft dysfunction after lung transplantation.
patients and require a multidisciplinary approach. American Journal of Transplantation. 2015;
15: 2188–2196.
• Post-transplant infections are common and the
microbiological history of both the donor and Singer JP, Diamond JM, Gries CJ, et al. Frailty phenotypes,
recipient is essential for their management. disability, and outcomes in adult candidates for lung
transplantation. American Journal of Respiratory and
• Numerous drug related complications are
Critical Care Medicine. 2015; 192: 1325–1334.
possible in the early postoperative period, and
detailed knowledge of drug interactions is Weill D, Benden C, Corris PA, et al. A consensus document
for the selection of lung transplant candidates:
important.
2014 –an update from the Pulmonary Transplantation
• Avoidance of renal dysfunction is important in Council of the International Society for Heart and
the early postoperative period as it can hinder Lung Transplantation. Journal of Heart and Lung
mobilisation and healing. Transplantation. 2015; 34: 1–15.
15:32:38
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346
MCQs
1. What is the 30- day and 1-
year survival post lung (c) Physiotherapy
transplantation? (d) Antibiotic resistance
(a) 99% and 85% (e) Multidisciplinary team management
(b) 90% and 85% 4. Which infections cause problems in lung transplant
(c) 85% and 60% recipients?
(d) 85% and 85% (a) Bacterial
(e) 90% and 70% (b) Viral
2. What is the leading cause of early mortality post lung (c) Fungal
transplantation? (d) Combined
(a) Infection (e) All of the above
(b) Primary graft dysfunction 5. Which of the immunosuppressant medications are
(c) Acute renal failure particularly vulnerable to drug interactions?
(d) Postoperative bleeding (a) NSAIDs
(e) Hepatic failure (b) Steroids
3. What factors make lung transplant patients particu- (c) Calcineurin inhibitors
larly vulnerable to infection? (d) Potassium supplements
(a) Poor sterility in the intensive care unit (e) Anticonvulsants
(b) The graft is open to infection and has impaired
immune defense
15:32:38
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347
Aortic Surgical Patients in the Intensive

Chapter
42 Care Unit
Pedro Catarino and Swetha Iyer
Introduction associated with medial degeneration in the aorta.

A number of conditions are known to predispose to
Aortic surgical patients in the ICU can be some of
these changes, including Marfan’s syndrome, Loeys–
the most challenging patients. Further, these are the
Dietz syndrome, Ehlers–Danlos syndrome, Turner’s
patients for whom good intensive care management
syndrome and bicuspid aortic valve. Vasculitides such
can make a big difference to the outcome. Most of
as giant cell arteritis and Takayasu’s arteritis are also
these patients are admitted to the ICU following an
predisposing conditions. In all cases, hypertension is
operation. Sometimes the patients may need to be
strongly implicated.
admitted to the ICU for preoperative optimisation.
Presentation is most commonly with chest pain,
Knowledge of the aortic disease pathology, the surgi-
described as severe and sharp and initially corre-
cal interventions for it, and the expected ICU support
sponding with the site of intimal tear then migrat-
is important for delivering optimal care for these com-
ing according to the extent of dissection of the aorta.
plex patients.
Syncope may occur, as may symptoms of malperfu-
sion. There may be signs of haemodynamic upset or
Aortic Pathology and Treatment indeed hypertension, as well as aortic regurgitation,
There are three main conditions requiring aortic cardiac tamponade and reduced pulses. The most
surgery. common differential diagnoses are myocardial infarc-
tion or pulmonary embolism. Diagnosis is urgent.
Aortic Dissection/Acute Aortic Syndrome An anatomical classification (Figure 42.1) under-
Aortic dissection forms part of a group of interrelated pins clinical management. The Stanford classification
pathologies where blood breaches the aortic lumen divides acute aortic dissection according to whether or
typically into the aortic media, to produce a so-called not the ascending aorta is involved, regardless of the
acute aortic syndrome. In aortic dissection there is an site of intimal tear. In type A dissection, the ascending
intimal tear. However, penetrating ulcer or rupture of aorta is involved and emergency open surgery is indi-
vasa vasorum (intramural haematoma) causes simi- cated in a cardiothoracic centre. This is an emergency
lar presentation and imaging. The blood in the media procedure with high (10–20%) operative mortality.
may track proximally or distally, producing a dissec- The goal of surgery is to excise the intimal entry tear
tion plane, which may rupture through the adventi- and direct blood down the true lumen by obliterat-
tia or back through the intima into the lumen again. ing the false lumen proximally. Frequently, dissection
The propagating dissection may also rupture into the extends down into the aortic root, causing prolapse of
pericardium, causing cardiac tamponade; it can dis- the aortic valve and regurgitation. Often reconstitut-
rupt the aortic valve, causing aortic regurgitation; or ing these layers with sutures and/or glue can resus-
impinge on side branches of the aorta causing malp- pend the aortic valve and so it does not need to be
erfusion syndromes (including cardiac ischaemia, replaced. If the root is already abnormal or irrepara-
stroke, intestinal or renal malperfusion and pulseless ble, then a root replacement is required, with or with-
limbs). out valve replacement depending on the condition of
Penetrating ulcer occurs in relation to athero- the aortic leaflets and the surgical expertise. Another
sclerosis and has similar risk factors. Intramural principle of the surgery is that the aorta, which is left
haematoma and acute aortic dissection are typically behind, should not have had a vascular clamp placed
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compression of surrounding structures). More typi-

cally, TAA is found incidentally on imaging for some
other indication. Symptoms may be a reason for
intervention, but more commonly size is the main
Intimal tear factor driving intervention. In these cases, the pre-
ar
al te
dicted risk of rupture or dissection (per annum) must

Intim
be balanced against the procedural risks (essentially

one time) in the individual patient. Limited natural
history studies have shown that the risk of an event
increases significantly at 6 cm for the ascending and
Type A Type B
7 cm for the descending aorta. In the absence of other
Figure 42.1 Classification of aortic dissection. factors therefore, a TAA of 5.5 cm in the ascending
aorta and of 6.5 cm in the descending aorta would
indicate intervention.
across it. This weakens the aorta, which is dissected
TAA is not a homogenous condition. The natural
and likely to be intrinsically abnormal. Therefore the
history varies according to the predisposing condi-
distal repair is performed ‘open’, i.e. without a clamp,
tion, and according to which segment of the thoracic
necessitating a period of circulatory arrest, which can
aorta is affected. TAA is commonly associated with
be partial or total.
aortic valve disease, coronary artery disease and
In type B dissection, the ascending aorta is not
abdominal aortic aneurysm. Thoracoabdominal aor-
involved and surgery is usually not indicated for
tic aneurysms are a particular form, which include
uncomplicated cases, which are typically managed by
thoracic and abdominal components, typically in con-
cardiologists in a CCU setting, with blood pressure
tinuity. The management of TAA is influenced by ana-
control and serial imaging until symptoms settle and
tomical factors, patient factors, pathological factors
imaging is stable. Complicated cases involve malper-
and institutional experience and is mostly decided by
fusion syndromes, ongoing pain or other suggestions
multidisciplinary teams.
of imminent rupture and then endovascular stenting
The options for management include the following:
is indicated in a vascular surgery unit.
Open Surgery
Thoracic Aortic Aneurysm (TAA) This involves resection of the aneurysm and replace-
The thoracic aorta is never normal at 4 cm in diameter ment of that segment with a polyester graft. Therefore
and this size serves as a pragmatic cut-off to diagnose that segment must be excluded from the circulation
TAA. Unlike abdominal aortic aneurysms, which are by vascular clamps or by arrest of circulation. For
commonly the result of atherosclerosis, this is much TAA of the ascending aorta, it is carried out through a
less likely in TAA, although TAA shares a number of median sternotomy with the patient on cardiopulmo-
risk factors with atherosclerosis, including hyperten- nary bypass. Adjunctive procedures on the heart are
sion, smoking and chronic obstructive pulmonary possible. It is also possible to deal with involvement
disease. TAA is also predisposed by connective tis- of the arch and/or proximal descending aorta, but this
sue defects due to a number of genetic syndromes or requires advanced perfusion techniques such as deep
inflammatory disorders. There is an association with hypothermic circulatory arrest or selective antegrade
congenital bicuspid aortic valves, which affects 2% of cerebral perfusion, and carries an additional risk of
the population. Atherosclerosis is more common in mortality, stroke, paraplegia and recurrent laryngeal
the descending thoracic aorta. nerve palsy. For TAA of the descending aorta, open
Since wall tension increases with greater diam- surgery is carried out via lateral thoracotomy. There
eter, TAA is an exponentially progressive condition are a number of surgical techniques to augment the
with the result that the aorta is increasingly at risk of distal aortic perfusion to reduce the risk of paraplegia
rupture or dissection. Patients occasionally present during clamping of the aorta, described below. Even
with symptoms such as change in voice (indicating with intercostal artery reimplantation, spinal cord
recurrent laryngeal nerve palsy), chest pain or short- ischaemia can occur, and adjuncts such as spinal cord
ness of breath, and even dysphagia (mostly down to drainage and motor evoked potentials may be used
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Chapter 42: Aortic Surgical Patients
to mitigate this risk. Patients need to have a degree of treatment. Associated injuries are common and may
physiological reserve to withstand this level of inva- complicate diagnosis and management.
siveness and achieve suitable recovery times. Most injuries (80%) occur at the aortic isthmus
just beyond the left subclavian artery. This is probably
Endovascular Stent Graft (ESG) because this area is the transition between the mobile
This involves exclusion of the TAA. A guidewire is ascending arch and the immobile descending aorta.
passed within the TAA, over which the ESG is passed Other locations include the transverse arch, proximal
from a peripheral artery, usually retrogradely. The ascending aorta and descending aorta just proximal
ESG is positioned under X-ray guidance and deployed, to the diaphragm. Rupture of the intima and media
resulting in exclusion of the aneurysm. A number of occurs at the time of injury and exsanguination is
different devices are used, which are generally con- prevented by the adventitia and surrounding tissues,
structed of a polyester graft supported by nitinol or but this remains at high risk without appropriate
stainless steel Z, which self-expand when deployed. management.
There are some anatomical requirements. First, the There are no specific symptoms or signs. A chest
proximal and distal landing zones should be at least radiograph may be suggestive, for example showing a
2 cm in length to ensure an adequate fixation and seal. widened mediastinum, but a normal physical exami-
In addition, the access vessels should be sufficiently nation does not exclude the condition. Chest CT is the
large to permit passage of the delivery system. There investigation of choice.
are ways of getting around both problems, such as per- The initial management is that of any trauma
forming extra-anatomical bypass or using branched patient, applying ATLS guidelines, whilst making the
or fenestrated stents to increase the potential landing diagnosis. If thoracic aortic injury is suspected then
zone, and using temporary surgical grafts to improve patients should be managed with a goal systolic blood
access to the aorta, but all these procedures add to the pressure of approximately 100 mmHg and a pulse of
complexity of the intervention. <100. Repair of blunt thoracic aortic injury can be
performed using open or endovascular techniques,
Medical Management with a growing preference for ESG.
There is limited evidence to support cessation of smok-
ing, blood pressure control and use of beta-blockers
and losartan in reducing the rate of aneurysm expan-
Anaesthetic and Critical Care
sion or events. Management
Other Issues Unstable Patients
Anatomical factors refer to the exact site with Acute type A aortic dissection is a surgical emer-
respect to branches of the aorta and the extent of gency. There is a 1% per hour mortality in the first
aorta involved. The site of the aneurysm determines 48 hours, with 50% of untreated patients dead by 1
the feasibility of both stent placement and/or clamp week. Transthoracic echo may show aortic regurgita-
placement in open surgery without compromising tion, pericardial effusion or even proximal dissection.
important aortic branches. Patient factors include age However, CT imaging provides the most definitive
and comorbidities, particularly respiratory and renal and reliable information and is indicated immediately
function. Pathological factors include whether there where there is clinical suspicion. Transoesophageal
is a connective tissue defect, the presence of infec- echo is best reserved for the anaesthetised patient
tion and whether the aneurysm is true or a chronic to prevent hypertensive surges, which could lead to
dissection. decompensation.
Acute rupture of TAA and aortic transection are
Thoracic Aortic Injury/Aortic Transection also unstable conditions mandating emergency inter-
Blunt aortic injury is common in trauma from major vention, and anaesthetic management is similar.
decelerating forces, typically road traffic accidents,
falls, or aeroplane crashes. The majority of patients die Preoperative
at the scene, but a significant proportion may reach Once the diagnosis is made, immediate transfer to a
hospital and may survive with timely diagnosis and cardiothoracic centre is indicated. In the meantime,
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blood pressure control is paramount. Admission to the right axillary artery (innominate artery clamped),
an intensive care unit should be considered for close or via separate catheters in the innominate artery
monitoring with insertion of an arterial line, wide- itself and/or the left carotid artery. The aortic root can
bore venous cannulae and urethral catheter. However, be operated on whilst the patient is cooling, or after
insertion of these lines should not delay transfer to the distal repair, whilst the patient is rewarming.
theatre or an accepting hospital.
Medical therapy has the goal of reduction of sys- Intraoperative monitoring: Monitoring must cover
temic arterial pressure while at the same time blunting the range of options for cannulation strategy since
the force of contraction of the heart (dP/dt), and hence the surgeon’s first choice may result in malperfusion,
the shear forces in the aorta. Intravenous Labetalol is which only becomes evident once instituted, and there-
the agent of choice, having both alpha-blocking (blood fore needs to be altered. Arterial monitoring proximal
pressure lowering) and beta-blocking (dP/dt lower- to the arch (right radial) and distal to the arch (left
ing) effects. Infusions of 0.5–2 mg/minute should be radial or femoral) is mandatory. It may be helpful to
administered, aiming for systolic BP 100–120 mmHg examine the CT to see whether the femoral arteries are
and heart rate of 60–70 beats/minute. Pain should be included, to determine whether they are dissected or
addressed with opiates as required. The patient should not. In the absence of CT guidance, the best pulse is
be monitored for evidence of malperfusion through usually chosen. Regardless of whether deep hypother-
ECG monitoring, recording neurological observa- mic circulatory arrest or selective antegrade cerebral
tions, attention to oliguria and abdominal pain, acid– perfusion is used, cerebral oximetry is required.
base changes and limb pulses.
Intraoperative management Stable Patients

The stable patients have time for careful discussion
The transition period from preoperative to intraop-
and planning between the surgeon, anaesthetist and
erative is hazardous for these patients. The priority for
perfusionist. The site of pathology determines the
the anaesthetist must be careful control of blood pres-
incision and options for perfusion.
sure and avoidance of worsening haemorrhage, which
can result in either cardiac tamponade or exsanguina- Ascending Aorta
tion. The priority for the surgeon will be institution
Surgery on the aortic root and/or ascending aorta,
of cardiopulmonary bypass. The anaesthetist and sur-
which does not involve the aortic arch, can be per-
geon must work together. If there is tamponade, then
formed with a single arterial line, usual central venous
great care should be taken at the time of pericardial
catheter, and does not require any of the advanced
opening, since an acute rise in blood pressure may fol-
adjuncts discussed below. Median sternotomy, or
low, producing exsanguination if bypass is not imme-
occasionally partial sternotomy is used; perfusion is
diately available.
mostly right atrial to ascending aortic bypass without
Numerous arterial cannulation strategies are feasi-
significant systemic hypothermia, and with standard
ble (Figure 42.2). The most common are right axillary
cardioplegic myocardial management.
artery or femoral artery or even carotid artery can-
nulation before sternotomy or direct aortic cannula- Aortic Arch
tion after sternotomy. Left ventricular apex and aortic
The role of anaesthesia and intensive care in these
cannulation after transection are also feasible. Almost
patients is to:
invariably, the right atrium is cannulated for venous
return, although in rare instances peripheral femoral • Facilitate surgery (positioning, perfusion and
venous cannulation may be preferred in order to com- equipment);
mence bypass prior to chest opening. • Ensure adequate organ protection/perfusion for
Cardiopulmonary bypass is instituted and moni- the heart, brain, spine, kidneys;
toring is observed to exclude induced malperfusion. • Prevent and allow aggressive management of
The patient is systemically cooled, to 18–20 °C for total coagulopathy;
circulatory arrest, or 22–28 °C for partial arrest. For • Minimise lung injury.
the latter, selective antegrade perfusion is continued, Since the supra- aortic vessels will be interrupted,
providing 10 ml/kg blood flow to the upper body via preparation for selective antegrade cerebral perfusion
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Right axillary artery

Right atrium Right atrium
1. Full cardiopulmonary bypass, cool to 25ºC 2. Clamp asc aorta, repair aortic valve,
replace asc aorta
Right atrium
3. Circulatory arrest to body, clamp innominate art

Selective antegrade cerebral perfusion 10 ml/kg/min 4. Distal anastomosis, rewarm,
Cut out clamp site asc aorta, reconstitute true lumen of arch off bypass
Figure 42.2 Variety of cannulation techniques for aortic surgery.
(SACP) is preferred, i.e. right radial and post-arch across the ascending aorta with perfusion line below
(left radial or femoral) arterial lines, cerebral oxime- this) with warm blood at 500–700 ml/min, which
try, and head cooling. Systemic hypothermia is invari- allows it to beat and avoids a prolonged ischaemic
ably used, either 22–28 °C for SACP or 18–20 °C if period. The ECG should be observed for adequacy of
total circulatory arrest is envisaged. this perfusion.
Bypass is typically right atrial to right axillary
artery. A second arterial perfusion line is prepared Descending/Thoracoabdominal Aortic Operations
which allows for either left carotid perfusion in the Operations on the descending thoracic aorta require
event that cerebral oximetry declines unacceptably, or left thoracotomy with the patient in a right lateral
for re-perfusion, once the arch graft is secured distally. decubitus position. If the abdominal aorta is also
Frequently there are concomitant cardiac proce- operated on then an extensive thoracolaparotomy is
dures requiring cardioplegia for myocardial manage- performed, cutting across the left diaphragm and cos-
ment. However, if there are not, or not during the arch tal margin. Double lumen endotracheal tube is pre-
part of the surgery, it is common to perfuse the heart ferred. There are a number of options for perfusion,
separately from the systemic circulation (i.e. clamp which is essential to maintain flow distal to any clamp
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below the aneurysm. Full cardiopulmonary bypass is

one option, with femoral venous outflow (long can-
Haemodynamics Goals
The majority of patients are likely to have normal ven-
nula up to the right atrium) and femoral artery + axil-
tricular function. Thus, hypotension is mainly associ-
lary artery inflow, i.e. perfusing above and below the
ated with hypovolemia and vasodilation. Maintaining
aneurysm. Partial cardiopulmonary bypass is an alter-
adequately high systemic arterial pressure and CVP is
native, with left atrial outflow (cannulation of either
important.
pulmonary vein or left atrial appendage) and inflow
If volume (i.e. cristaloids and blood products)
to the femoral artery or distal descending aorta.
does not achieve the above mentioned goals, then a
Therefore the left heart is only partly drained, so that
rather early introduction of vasoconstrictors should
the heart ejects blood into the upper body including
be aimed for, to minimise the episodes of sustained
the coronaries, above any proximal clamp, and the
hypotension.
bypass circuit pumps already oxygenated blood dis-
Cardiac tamponade is less common in these
tal to any distal clamp. There is no oxygenator in the
patients. However, echocardiographic exam should be
circuit, so less heparin is required, and the perfusion
considered in patients with poor response to vasocon-
is normothermic so that the heart continues to beat
strictors and volume administration.
normally. For both these forms of cardiopulmonary
Maintaining normothermia is important, unless
bypass, separate perfusion lines can be taken off the
the theatre team advise otherwise based on intraoper-
arterial line to continuously perfuse the coeliac axis,
ative events. Hyperthermia increases the risk of spinal
superior mesenteric artery and both renal arteries, in
injury and should be treated actively. Mild hypother-
the case of thoracoabdominal procedures.
mia (35.5–36.4 °C) can be accepted if the patient has
A final option for straightforward cases is a Gott
good haemostasis.
shunt where the aortic arch is cannulated above the
Mechanical ventilation should be adjusted as per
proximal clamp and the distal aorta cannulated below
ICU protocol.
the distal clamp and these are connected with a short
piece of heparin- coated tubing providing passive
shunting to the distal aorta. Spinal Cord Protection via CSF
Right radial arterial lines for the upper body and
femoral arterial lines for the lower body are essential.
Drainage
Although the evidence behind this approach is not
Spinal cord drain and motor evoked potentials are
robust, many aortic centres use spinal catheters to
important adjuncts for addressing interruptions to
drain SCF in an attempt to increase spinal perfusion
spinal cord perfusion.
pressure and reduce the risk of spinal cord damage.
The spinal catheters are normally placed in the operat-
General ICU Goals for Management of ing theatres; however, in rare cases when they are not
used intraoperatively, and the patient wakes up para-
Aortic Surgical Patients plegic, a spinal catheter can be inserted in the ICU as a
last attempt to reverse permanent paraplegia.
Perioperative Coagulopathy
Management Spinal Cord Drainage
Persistent bleeding is common and it can lead to epi- Paraplegia remains one of the most devastating com-
sodes of hypotension, which may increase the risk of plications of thoracic aortic surgery and is associated
spinal cord injury. Proactive coagulation manage- with a significant increase in both morbidity and mor-
ment allows maintaining higher systemic perfusion tality. One of these modalities that acts via optimising
pressure without excessive increment in the risk of spinal cord blood flow is lumbar cerebrospinal fluid
bleeding. If coagulopathy is suspected or confirmed, (CSF) drainage. The purpose of the drain is to allow
conventional blood products should be used as per control of the CSF pressure and help maintain blood
ICU protocols. If bleeding persists despite a first flow up and down the anterior spinal artery. During
round of FFP, PLTs and cryoprecipitates/fibrinogen, the course of resecting a thoracoabdominal aneurysm,
a surgical review is required and the haematologist various vessels (intercostal arteries) that contribute to
should be contacted. the anterior spinal artery are transected. Some of these
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353
Hanger hole Flow chamber

locking bracket
System mounting panel Hydrophobic filtervent

Cord lock
Instructions for use
Flow chamber Arrow
Pressure scales
Stopcock Sliding graduated
drip chamber
Patient line stopcock
injection site Slide clamp
(Optional transducer
adapter location) Drainage line
injection site
End plug Flow chamber
connection line
Main system stopcock Drainage bag
connection line
Main system Slide clamp

end plug
(Optional transducer
adapter location)
Microbial filter and
Patient connection line drain port cap
One-way valve
Drainage bag
Figure 42.3 Spinal drain monitoring system.
vessels will be reattached to the graft that replaces the anaesthesia. A key consideration is the ability to
aorta, but it is not possible to do this with all of them. provide controlled hypotension at the time of stent
The insertion of the spinal catheter should be car- deployment, and/ or balloon inflation, minimis-
ried out under strict and full aseptic conditions by ing malposition, followed by relative hypertension
the anaesthetist. The system (Figure 42.3) should be once the stent is positioned. This can be achieved by
calibrated (zeroed) independently of all other pressure administration of adenosine, which causes a transient
transducers. This should be performed at the level of the heart block. The usual dose is 36 mg of adenosine
phlebostatic axis (location of right atrium) with the bed (18 mg for subsequent episodes), which produces 4–6
flat. The target CSF pressures are kept between 10 and seconds of cardiac asystole. Rapid pacing is another
12 mmHg immediately following surgery and 12 and method to lower the cardiac output briefly. A tem-
15 mmHg once the patient is awake and moving. porary transvenous pacing electrode placed via the
jugular vein before the procedure allows for rapid
pacing at 160–180 beats/minute. After deployment,
Anaesthesia and ICU for ESG the rapid pacing is stopped, and the blood pressure
Thoracic endovascular aortic repair (TEVAR) can is recovered. Hypertension once the stent is in place
be performed under general, regional or local is aimed at enhancing spinal cord perfusion. Since a
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good number of intercostal arteries are covered by the delayed blood product administration leads to
stent, spinal cord drainage should also be considered wasting of the already administered coagulation
prior to the procedure. This is indicated for extensive factors.
coverage, coverage without revascularisation of the
left subclavian artery and previous abdominal aortic Further Reading
surgery.
Erbel R, Aboyans V, Boileau C, et al. 2014 ESC
Guidelines on the diagnosis and treatment of aortic
Other Forms of Aortic Surgery diseases. European Heart Journal. 2014: 35:
Coarctation or aberrant aortic vessels are also oper- 2873–2926.
ated on and the same principles apply according to Fedorow CA, Moon MC, Mutch WA, Grocott HP. Lumbar
the anatomical site of the procedure. Typically these cerebrospinal fluid drainage for thoracoabdominal
patients are younger and have better than average tis- aortic surgery: rationale and practical considerations
sues and physiological reserve. for management. Anesthesia & Analgesia. 2010;
111: 46–58.
Foley LS, Yamanaka K, Reece TB. Arterial cannulation and
Learning Points cerebral perfusion strategies for aortic arch operations.
• Aortic surgery is complex, and it can be elective Seminars in Cardiothoracic and Vascular Anesthesia.
or emergency. In emergency operations, timing of 2016; 20: 298–302.
diagnosis, transfer and treatment is crucial. Griepp RB, Griepp EB. Spinal cord protection in surgical
• Anaesthesia and intensive care can make a and endovascular repair of thoracoabdominal aortic
significant difference to patient outcome of aortic disease. Journal of Thoracic and Cardiovascular Surgery.
surgical patients. 2015; 149: S86–S90.
• Spinal cord drain and motor evoked potentials are Lee AW. Status of branched grafts for thoracic aortic arch
important adjuncts for addressing interruptions endovascular repair. Seminars in Vascular Surgery.
2016; 29: 84–89.
to spinal cord perfusion.
• The general ICU goals for management of aortic Matsuda H. Treatment of uncomplicated type B aortic
dissection. General Thoracic and Cardiovascular
surgical patients are: coagulopathy management,
Surgery. 2017; 65: 74–79.
blood pressure management and spinal cord
protection. Wynn MM, Acher CW. A modern theory of spinal cord
ischemia/injury in thoracoabdominal aortic surgery
• Bleeding following aortic surgery is common and and its implications for prevention of paralysis. Journal
it should be treated expectantly. Coagulopathy of Cardiothoracic and Vascular Anesthesia. 2014;
is common and should be treated promptly as 28: 1088–1099.
MCQs
1. The role of anaesthesia for aortic surgery is to: (b) Aortic root
(a) Facilitate surgery (positioning, perfusion and (c) Descending aorta
equipment) (d) Aortic arch
(b) Ensure adequate organ protection/perfusion for the (e) Thoracoabdominal aorta
heart, brain, spine, kidneys
3. Use of vasopressors in postoperative surgical patients:
(c) Prevent and allow aggressive management of
coagulopathy (a) Is contraindicated as it reduces organ perfusion
(d) Minimise lung injury (b) Allows maintaining perfusion pressure
(e) All of the above (c) Should be initiated prior to fluid administration
2. The risk of spinal cord injury during aortic surgery is (d) Is more important than blood product administration
highest in operations involving: (e) Should be used to provide supraphysiological
(a) Ascending aorta perfusion pressure
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4. CSF drainage for spinal cord protection: 5. Spinal cord damage following aortic surgery:
(a) Should be used in all cardiac surgical patients (a) Occurs only after open operations
(b) Carries a risk of meningitis (b) Can be reliably prevented by CSF drainage
(c) Commonly produces dural puncture (c) Can be prevented by intraoperative perfusion
headache techniques
(d) Renders epidural analgesia contraindicated (d) Is the most devastating complication of surgery
(e) Should only be done preoperatively (e) None of the above
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Thoracic Surgical Patients

Chapter
43 J Irons and S Ghosh
Introduction dedicated thoracic surgical ward and do not recom-

mend the routine admission of high-risk patients to
In the UK, 26,746 thoracic surgical procedures were
ICU. In the presence of an appropriate HDU, no tho-
recorded in the Society of Cardiothoracic Surgeons
racic surgical patient should be admitted to ICU elec-
Thoracic Registry as having been performed in 2013–
tively; only those patients who require organ support
2014. Of these procedures, 6713 were primary lung
as an emergency measure should be considered for
cancer resections.
ICU admission. Examples of valid indications for ICU
The association between lung cancer, smoking,
admission in this group of patients include mechani-
emphysema and cardiovascular disease is widely
cal ventilation for acute respiratory support, haemo-
accepted and thus thoracic surgical patients often have
filtration for acutely deteriorating renal function or
significant comorbid conditions. The preponderance
inotropes for acute cardiac failure.
of comorbid disease, together with the extent of sur-
gery and the surgical approach, predispose to numer-
ous potentially serious complications. Perioperative Mortality
management of thoracic surgical patients should focus Mortality following lung resection has significantly
on the utilisation of techniques that promote early improved over the years with improved diagnostic
mobilisation and discharge. Key factors in achieving and treatment strategies. The overall mortality rate
this aim are as follows: for lung resection in the UK in 2013–2014 was 1.7%.
Pneumonectomy carried a higher mortality rate at
• Optimisation of lung function preoperatively,
5.9% compared to open lobectomy at 2%, which
for example by physiotherapy and treatment of
in turn carried a higher mortality rate than VATS
infection or oedema/effusions
lobectomy at 0.7% and VATS wedge lung resections
• Improving nutritional status preoperatively
at 0.18%.
• Limiting intraoperative lung injury, for example The most frequent cause of death is acute respira-
due to barotrauma or excessive fluid infusion tory distress syndrome (ARDS), followed by bron-
• Prompt return to spontaneous ventilation at chopleural fistula (BPF) and empyema, cardiac events
the end of the procedure to reduce barotrauma, and cerebrovascular accidents.
nosocomial infection and prolonged air leaks
perpetuated by positive pressure ventilation
• Use of adjunctive intraoperative and
Reduction of Complications and
postoperative analgesic techniques, for example Mortality
central or peripheral nerve blocks, to ensure the A number of recent advances in thoracic surgery have
patient is sufficiently pain free to cough and clear led to a reduction in the number of complications and
secretions. mortality.
Routine admission of patients to intensive care and
high dependency units can lead to delay in patient Video Assisted Thoracic Surgery (VATS)
mobilisation and recovery, increased nosocomial Lobectomy remains the most commonly carried out
infections, bed occupancy issues and increased costs. lung resection procedure but there is a definite shift in
The European Society of Thoracic Surgery (ESTS) the surgical approach towards minimal access (VATS)
states that low-risk patients should be admitted to a surgery. Provisional figures for 2013–2014 in the UK
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Chapter 43: Thoracic Surgical Patients
show 30% of lobectomies for lung cancer were car-

ried out using a VATS approach (increasing from 23%
Enhanced Recovery
The adoption of enhanced recovery programmes for
in 2012–2013). The adoption of VATS techniques in
thoracic surgery has served to increase throughput
thoracic surgery has driven improved patient out-
and decrease hospital length of stay. The enhanced
comes including survival, reduced complications and
recovery programme aims to institute a number of
a shorter recovery. However, as a result, increasingly
evidence-based interventions in order to assess and
complex surgical procedures are now being per-
optimise the patients preoperatively, reduce the stress
formed on older and sicker patients.
associated with the surgery and promote recovery and
restoration of normal function. These programmes
Pleural Drainage have led to a decrease in complications and ICU
Advances in chest drain technology and the under- admissions, as well as a reduction in hospital length of
standing of the management of pleural spaces has stay. The enhanced recovery programme recommen-
greatly advanced. There has been an introduction of dations for thoracic surgery are listed in Table 43.1.
chest drains with digital quantification of leaks and Within the enhanced recovery programme, the
pleural pressures, the use of miniature dry suction aim of preoperative assessment and optimisation is
chambers with one-way valves which have improved to identify patients at risk of complications and where
safety and allow easy early mobilisation with a shoul- possible take measures to prevent such complications
der strap. The avoidance of suction and early removal from arising. Specific risk factors have been identified
have allowed earlier discharge. In the case of pro- in the development of postoperative complications:
longed air leaks, discharge with a chest drain in situ,
• Age >75
reviewed 2–4 weeks later, has decreased length of stay
and reoperation rate. • Male sex
Following pneumonectomy, the space within the • Smoker or ex-smoker
pneumonectomised hemithorax gradually fills with • COPD
fluid over a period of days to weeks (see Figure 43.1). • Interstitial lung disease
In the immediate postoperative period close clinical • Concurrent cardiac disease
and radiological monitoring is required for signs • Lung function FEV1 <60%, TLCO <50%.
of accumulation of blood or air and for mediasti-
nal shift, i.e. movement of the mediastinal con-
tents from their midline position as a result of
Analgesia
Thoracotomy ranks amongst the most painful of sur-
changes in intrathoracic pressure. This cavity can be
gical procedures. The constant motion of respiration
managed with:
and coughing compounds the pain from muscles that
• No drainage have been transected or overstretched and torn, and
• Underwater seal drain clamped and released ribs that have been partially excised or fractured dur-
intermittently to allow assessment of blood loss ing thoracotomy. The surgical technique can be modi-
and release any trapped air fied to reduce the severity of pain, for example by
• Balanced pleural drainage (injection/aspiration of avoiding rib fracture or resection or performing the
air to limit mediastinal shift). procedure by VATS rather than thoracotomy.
The use of balanced pleural drainage may be asso- Pain relief after thoracic procedures can be
ciated with a lower incidence of mediastinal shift and achieved in many ways, including systemic analge-
postoperative ARDS. This may be because limitation sics, epidural analgesia, paravertebral or intercostal
of movement of the heart and pulmonary vessels from blocks, intrapleural regional anaesthesia or cryoanal-
their usual position reduces changes in transpulmo- gesia. Ineffective analgesia often results in poor chest
nary vascular pressures in the remaining lung and so expansion and expectoration, leading to atelectasis
decreases the propensity for the development of pul- and chest infection. Multimodal analgesia combining
monary oedema. Or it may be that maintenance of the systemic non-opioid and opioid analgesics together
mediastinal contents in their midline position reduces with some form of nerve block is regarded as the most
the mechanical stresses on the residual lung caused by effective means of rendering the patient comfortable,
over-distension or compression. but without over-sedation.
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(a) (b)
(c) (d)
Figure 43.1 Sequential chest X-rays from a post-pneumonectomy patient demonstrating normal filling of the left hemithorax. (a) Day of
surgery, (b) day 1, (c) day 4, (d) day 8.
Table 43.1 Enhanced recovery recommendations
Preoperative Admission Anaesthesia Surgery Postoperative

Identify and treat anaemia Same day admission Appropriate antibiotic VATS if possible DVT prophylaxis
prophylaxis
Nutrition support Avoid premedication Short acting agents Single chest drain if Avoid drain suction
possible
Smoking cessation Minimise fasting Protective ventilation Early drain removal
Medical therapy DVT prophylaxis Avoid fluid overload Early mobilisation
optimisation
Physiotherapy Consider AF prophylaxis Paravertebral analgesia Physiotherapy
prehabilitation preferred to epidural
Risk calculation Early extubation
Education regarding stay,
recovery and discharge
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Thoracic epidural analgesia has been the main- • Cardiac dysfunction

stay of thoracic anaesthetic practice for many years • Pulmonary embolism
and provides arguably the best postoperative pain • Bleeding
relief. Although epidural infusions have been shown • Bronchopleural fistula.
to reduce the incidence of chest infection, large num-
bers of complications have been attributed to epidural
insertion and to the management of epidural infu-
ARDS Post Lung Resection
Pulmonary complications are a major cause of mortality
sions. Serious complications include nerve injury,
and morbidity following thoracic surgery, with ARDS
epidural abscess and haematoma –the routine use of
the leading cause of death. The incidence and severity
low molecular weight heparin for thromboprophy-
of ARDS is related to the extent of pulmonary resection,
laxis and burgeoning use of novel oral anticoagulant
with pneumonectomy posing a risk of 3–10% while a
agents making the latter a significant concern. Other
lesser resection poses a risk of only 2–5%. Mortality in
significant disadvantages are hypotension due to con-
those who develop ARDS is as high as 25–60%.
comitant sympathetic block, requiring the use of intra-
One-lung ventilation is non-physiological and will
venous fluids or vasopressors, and delay in patient
result in some degree of lung injury. Over-hydration
mobility and, therefore, recovery and discharge.
and high tidal volumes were traditionally thought to
These factors have led to the search for alternative
be the cause of the damage; however, it is now known
safer techniques of regional block. The most com-
that the mechanism is more complex and multifacto-
monly used techniques today are paravertebral block,
rial and occurs in both the ventilated and collapsed
or intercostal nerve block. The analgesic efficacy of
lung for different reasons.
these techniques may often not be as great as that pro-
In the ventilated lung, damage occurs from venti-
vided by an epidural infusion, but complications are
lator induced lung injury with high pulmonary pres-
certainly reduced and the patient is able to mobilise
sures and tidal volumes along with loss of functional
quicker and can be discharged sooner. Paravertebral
residual capacity and hyperperfusion. The collapsed
blocks can be placed either as single shot blocks at
lung is affected by surgical manipulation and resec-
multiple levels or via placement of a catheter with
tion along with ischaemia- reperfusion injury and
an infusion of local anaesthetic for longer or more
sheer forces from lung re-expansion. The resultant
complex procedures. Paravertebral catheters may be
reactive oxygen species and cytokines released into
placed by the anaesthetist at the beginning of the pro-
the circulation then act to cause injury in both lungs.
cedure, or placed directly by the surgeon at the end
This cumulates in damage to the endothelial glycoca-
of the procedure. Multilevel intercostal nerve blocks
lyx with vascular leakage and cell migration.
are also commonly utilised and are effective at con-
There is no single pre-emptive measure that has
trolling acute pain, but usually are only effective for
shown to be beneficial in preventing the develop-
up to 4–6 hours.
ment of ARDS. Studies indicate, however, that lower
tidal volumes (4–5 ml/kg), the addition of a moderate
Thromboprophylaxis amount of PEEP (5–10 cmH2O), avoiding hyperoxia
Evaluation of venous thromboembolic risk in all and the use of recruitment manoeuvres can help to
patients and the routine use of pharmacological and reduce atelectasis, acute lung injury, ICU admission
non-pharmacological prevention has significantly and hospital length of stay. PEEP may, however, exac-
decreased the incidence of morbidity and death erbate and delay spontaneous resolution of air leaks
from thromboembolic disease in thoracic surgical from the lung surface and PEEP should be applied
patients. judiciously if air leak is observed from pleural drains
during positive pressure ventilation.
Complications Post Thoracic Surgery Surgical factors predisposing to the development
Common complications post thoracic surgery include: of ARDS include:
• ARDS • Extent and duration of surgery
• Air leak and pneumothorax • Pneumonectomy (R>L, carinal>non-carinal)
• Sputum retention and atelectasis • Intraoperative and postoperative fluid load
• Arrhythmias • Volume of blood loss
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• Administration of blood products Bronchopleural Fistula

• Non-balanced hemithorax drainage
A bronchopleural fistula (BPF) is a significant cause of
post-pneumonectomy.
morbidity and mortality following thoracic surgery. It
Post-extubation, non-invasive ventilation (NIV) and is a persistent communication between the bronchial
high flow nasal oxygen therapy have been shown stump and the pleura, resulting in a persistent air leak.
to improve lung mechanics and oxygenation and The incidence is approximately 0.5% after lobectomy
are beneficial in those at high risk of respiratory and 4.5–20% after pneumonectomy, more commonly
complications. following right pneumonectomy. It is most often diag-
The treatment strategies for ARDS post thoracic nosed at day 7–15 postoperatively.
surgery are similar to those in general: The fluid filled pleural space may become infected
• Consider NIV and aspirated into the airway, leading to sepsis and
• Invasive ventilation should comprise low tidal respiratory compromise. Onset of breathlessness,
volume, low peak airway pressure, PEEP applied exacerbated in the supine position, a low grade
at a level commensurate with minimising pyrexia and blood stained expectoration are the clas-
persistent air leak via pleural drains sical presentation, although it may present as a ten-
• Permissive hypercapnoea sion pneumothorax and cardiorespiratory collapse.
• Avoid hyperoxia The typical radiological finding is an air-fluid level
• Balanced pleural drainage, for prevention of within the pneumonectomised hemithorax, with
mediastinal shift following pneumonectomy repeat chest radiographs showing a falling fluid level
• Appropriate antibiotic use (see Figure 43.2) and CT scan may demonstrate a
hydropneumothorax, pneumomediastinum and in
• Conservative fluid management
a few cases the actual fistulous communication (see
• Avoid blood products due to risk of transfusion
Figure 43.3).
related lung injury (TRALI)
Emergency surgical treatment is often required
• Use of ICU care bundles, for example DVT
with repair of the stump with an omental or muscle
prophylaxis, sedation breaks, CVP line care.
patch. More recently, the uses of tissue glue, fibrin or
valves applied bronchoscopically to seal the defect
Air Leak and Pneumothorax have been advocated. Thoracoplasty to occlude the
Air leak is a common problem after thoracic surgery. pneumonectomy space may also be considered.
Following lung resection, the residual tissue usually Intubation and positive pressure ventilation may
expands and fills the pleural space. However, if there be required to manage respiratory distress accom-
are damaged areas on the lung surface these can com- panying sepsis or for surgical closure of the fistula.
municate with the pleura, causing air leak via the Induction and intubation in this situation can be chal-
chest drain or a pneumothorax in the absence of an lenging, as the patients may be hypoxic, haemody-
effective patent drain. The air leak can be either an namically unstable and distressed. In the absence of
alveolar-pleural fistula, due to an open communica- a chest drain, there is a risk of tension pneumothorax
tion with lung parenchyma, or a bronchopleural fis- during positive pressure ventilation; furthermore, the
tula, due to a communication between a bronchus application of positive pressure may fail to produce
and pleura. adequate ventilation if large volumes of inspired gas
Management is usually conservative. The alveolar- are lost through the fistula and may also exacer-
pleural fistulae often seal over the first few days. This bate spill-over of the infected pleural fluid into the
is aided by spontaneous ventilation and applica- bronchial tree as gas is forced into the pleural cavity
tion of negative pressure suction to chest drains. If displacing fluid.
suction is applied too vigorously, however, it may Inhalational induction and subsequent lung isola-
perpetuate the air leak and in some cases cause respir- tion with a double lumen endobronchial tube in the
atory compromise as a result of loss of tidal volume. semi-erect position offer good protection against lung
Prolonged air leak after lung resection is associated soiling with infected fluid and avoid positive pressure
with an increased complication rate and prolonged ventilation to the bronchial stump. However, inhala-
hospital stay. tional induction to the depth of anaesthesia required
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361
achieve in practice. The use of rapid sequence induc-

tion and intubation has been advocated as offering
a more rapid means of securing the airway. Awake
fibreoptic endobronchial intubation has also been
described in this situation.
Medical management involves dependent drain-
age, appropriate antibiotics, low pressure ventilatory
support to promote healing without compromising
gas exchange, physiotherapy and good nutrition.
Sputum Retention, Atelectasis and Chest

Infection
Poor respiratory reserve, combined with inadequate
analgesia and infrequent physiotherapy, often leads
to atelectasis and respiratory tract infection (see
Figure 43.4). The incidence of pneumonia after tho-
racic surgery is 5–25%, and carries a mortality of
around 20%. The preoperative predictors include
Figure 43.2 Chest X-ray demonstrating a drop in the air-fluid level
old age, chronic obstructive pulmonary disease, sig-
in the absence of a chest drain. nificantly reduced forced expiratory volume and pro-
longed/extensive surgery. Common pathogens are
Haemophilus, Streptococcus, and Pseudomonas. The
best treatment is probably prevention, but once estab-
lished the infective complications should be treated
promptly with appropriate antibiotics after culture,
effective analgesia and physiotherapy.
Cardiac Dysfunction
Arrhythmias
The commonest arrhythmia following lung resection
is atrial fibrillation (AF). The incidence of AF ranges
from 12 to 44%. Patients who develop AF are more
likely to develop other complications and it is associ-
ated with a longer hospital stay and higher mortality.
Risk factors for the development of AF include:
• Male sex
• Older age
• Extent of surgery (higher incidence following
Figure 43.3 CT scan demonstrating a bronchopleural fistula post pneumonectomy)
right pneumonectomy. Note the right-sided hydropneumothorax
with air extending into the mediastinum creating a • Pre-existing cardiac disease, in particular
pneumoperitoneum and decompressing into the subcutaneous congestive cardiac failure and previous AF
tissues. • Length of procedure
• Pericardial involvement or inflammation.
for passage of an endobronchial tube can be accom- In one-third of the patients who develop AF, the onset
panied by cardiovascular compromise, particularly in is associated with chest infection or sepsis. It is most
septic, unstable patients, and can be difficult to safely prevalent on the second and third postoperative day.
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362
(a) (b)
Figure 43.4 Sequential chest X-rays of a patient post left lower lobectomy who developed sputum retention and collapse/consolidation of
remaining right lower lobe postoperatively. (a) Day of surgery, (b) day 2.
The Society of Thoracic Surgeons published rec- Digoxin should not be used as a primary agent for rate
ommendations on the prophylaxis and treatment of control, but can be used in combination if other rate
AF related to general thoracic surgery. Due to the control measures fail.
high morbidity and mortality and costs related to Prophylactic anticoagulation with low molecular
AF, prophylaxis should be considered in higher risk weight heparin is recommended as an early measure
patients. Beta-blockers and diltiazem are the drugs during the acute phase postoperatively to prevent the
of choice for prophylaxis. There is some evidence development of thrombus in the left atrial appendage
that amiodarone may be beneficial prophylactically, if the patient has two or more risk factors for stroke.
but should be avoided in pneumonectomy patients This should be converted to warfarin in the longer
because of the pulmonary side effects associated with term if AF persists. If the patient is at low risk of
amiodarone. Magnesium is useful as an adjunctive stroke, aspirin is recommended.
measure for the short- term management of acute
atrial fibrillation and ensuring that plasma magne- Myocardial Ischaemia
sium and potassium levels are within normal ranges Perioperative myocardial ischaemia and infarction,
may reduce the risk of developing AF. There is no evi- a commonly feared complication, is rarely reported
dence that prophylactic digitalisation is of benefit and in the literature and there is a scarcity of data on
so it should not be used. the current incidence. In a large historical study of
The treatment of AF, once it has occurred, can be postoperative thoracotomy patients, the incidence
pharmacological rate or rhythm control or synchro- of ECG changes indicative of myocardial ischaemia
nised direct current (DC) cardioversion. The choice was reported as 3.8% and myocardial infarction 1.2%.
depends on haemodynamic stability and symptoms. The perioperative factors most strongly predictive of
In the haemodynamically unstable patient, DC cardi- ischaemic events were poor preoperative exercise tol-
oversion is recommended. In the haemodynamically erance and intraoperative hypotension.
stable patient, if symptoms are intolerable, pharma- Thoracic surgical patients often have concomitant
cological cardioversion should be considered with cardiac risk factors or overt cardiac disease and rigor-
amiodarone or flecainide. If symptoms are tolerable, ous preoperative assessment and selection can limit
rate control with beta-blockers, or diltiazem if beta the incidence of postoperative morbidity and mortal-
blockade is contraindicated due to COPD or bron- ity ascribable to myocardial ischaemia and infarction.
chospasm, should be first line treatment in the first The American College of Cardiology and American
24 hours together with optimisation of electrolyte sta- Heart Association guidelines for perioperative evalu-
tus (magnesium, potassium and acid–base balance). ation and management for non-cardiac surgery is a
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363
useful resource, thoracic surgery being classified as be informative. The indications for re-thoracotomy
high risk in the context of that guidance. Coronary are rapid blood loss, a large intrathoracic collection or
angiography should be performed in the presence of persistent hypoxia due to compression of the lung or
major clinical predictors, i.e. unstable angina, heart pulmonary veins.
failure, arrhythmias or valvular disease. In patients
requiring preoperative stenting, surgery should be
postponed for 2–4 weeks. Patients who are consid-
Learning Points
• Postoperative thoracic surgical patients should
ered at risk of myocardial ischaemia should ideally
not be admitted routinely to the ICU; only
be invasively monitored intraoperatively and post-
those patients who require organ support as an
operatively. Appropriate measures should be taken to
emergency measure should be considered for ICU
maintain cardiac filling pressures and arterial blood
admission.
pressure at optimum levels and consideration given to
• Morbidity and mortality following thoracic
the use of inotropes, vasopressors or vasodilators to
surgery has significantly improved over the last
prevent or limit the sequelae of ischaemic myocardial
few years with the increase in minimal access
dysfunction.
surgery, advances in equipment and drainage
systems, development of enhanced recovery
Right Heart Failure
programmes, thromboprophylactic protocols and
Theoretically the strain on the right ventricle should improvement in analgesic strategies.
increase with the increase in afterload following lung • ARDS remains the leading cause of death
and pulmonary artery resection. However, the right following thoracic surgery and protective
ventricular end- diastolic pressure in fact remains lung strategies should be routine in patients
stable in the first few hours postoperatively, and only undergoing one-lung mechanical ventilation.
increases significantly on the first and second day. PEEP should be applied judiciously during
As concomitant cardiac disease is not uncommon in positive pressure ventilation at a level
patients undergoing lung resection, postoperative car- commensurate with minimising persistent air
diac failure is a possibility and preventative measures leak via pleural drains.
such as careful monitoring of fluid balance need to
• Patients with a bronchopleural fistula may present
be taken.
as an emergency due to a tension pneumothorax
Pulmonary embolism and heart herniation are
or due to respiratory compromise or sepsis. They
rare causes of RV decompensation but carry very high
can present a considerable challenge for induction
mortality following lung resection. Heart herniation
and intubation.
may occur if the pericardium is opened intraopera-
• AF post thoracic surgery is common and is
tively and not adequately closed.
associated with a higher morbidity, mortality and
hospital length of stay. High-risk patients should
Bleeding be considered for prophylaxis.
Bleeding is a rare complication after thoracic proce-
dures with an incidence of 0.1–3% of thoracotomies
and 2% of VATS cases, with re-exploration rates for
Further Reading
haemostasis in less than 1.9% and 1% respectively. De Decker K, Jorens PG, Van Schil P. Cardiac
Most bleeding is secondary to technical problems, complications after noncardiac thoracic surgery: an
evidence-based current review. Annals of Thoracic
although patient comorbidities and medication may
Surgery. 2003; 75: 1340–1348.
be predisposing factors. Meticulous attention to intra-
Fernando H, et al. The Society of Thoracic Surgeons
operative haemostasis and correction of coagulopathy
Practice Guideline on the prophylaxis and
are thus essential. management of atrial fibrillation associated with
Bleeding is usually from the lung parenchyma, general thoracic surgery: executive summary. Annals of
bronchial vessels or intercostal arteries. It is usually Thoracic Surgery. 2011; 92: 1144–1152.
detected from the effluent chest drainage, but chest Jones NL, Edmonds L, Ghosh S, Klein AA. A review
drains may become blocked and in the presence of of enhanced recovery for thoracic anaesthesia and
hypotension and tachycardia a chest radiograph may surgery. Anaesthesia. 2013; 68: 179–189.
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Lohser J, Slinger P. Lung injury after one lung ventilation: a The SCTS Thoracic Surgery Audit Group. The Thoracic
review of the pathophysiologic mechanisms affecting Surgery Registry Brief Report: Audit Years 2011–12 to
the ventilated and collapsed lung. Anaesthesia & 2013–14. Society for Cardiothoracic Surgery in Great
Analgesia. 2015; 121: 302–318. Britain and Ireland.
MCQs
1. Following lung resection, which of the following are (c) Permissive hyperoxia
common complications? (d) Conservative fluid management regimens
(a) Air leak via pleural drains (e) Low tidal volumes and conservative fluid
(b) Atrial fibrillation management
(c) Acute lung injury 4. Regarding bronchopleural fistulae (BPF) which of the
following are true?
(d) Sputum retention and atelectasis
(a) BPF most commonly occurs after left lung
(e) All of the above lobectomy
2. Risk factors for post lung resection complications (b) BPF is usually diagnosed within the first 24 hours
include which of the following? postoperatively
(a) Age (c) Symptoms include a high temperature
(b) Concurrent cardiac disease (d) Breathlessness and expectoration of blood tinged
(c) On lung function tests: FEV1 > 60%, TLCO > 50% sputum are exacerbated when sitting upright
(d) Extent of lung resection (e) None of the above
(e) (a), (b) and (d) 5. Recommendations for the management of atrial fibril-
lation (AF) in thoracic surgical patients include:
3. Which of the following are beneficial in managing
ALI/ARDS? (a) Prophylaxis with digoxin in high risk patients
(a) IPPV with tidal volumes of 9–10 ml/kg and PEEP (b) Amiodarone for pharmacological cardioversion
of 5 cmH2O (c) Rate control with either beta-blockers or diltiazem
(b) IPPV with tidal volumes of 4–5 ml/kg and PEEP of (d) The use of aspirin in all patients who develop AF to
8–10 cmH2O reduce the risk of stroke
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Section 7
Disease Management in the Cardiothoracic Intensive Care
Unit: Incidence; Aetiology; Diagnosis; Prognosis; Treatment
Chapter
Respiratory Disorders: Acute Respiratory
44 Distress Syndrome
Alastair Proudfoot and Charlotte Summers
Definitions and Epidemiology person-years, with an in-hospital mortality rate of

38.5%. Other data suggest that the incidence of ARDS
Acute respiratory distress syndrome (ARDS) is char-
may have declined since the 1990s. The decline in
acterised by acute inflammation affecting the gas
incidence has been attributed to improvements in
exchange surface of the lung, presenting clinically
healthcare delivery and process, including adherence
with acute hypoxaemia, in the presence of bilateral
to low tidal volume ventilation, and early recognition
pulmonary infiltrates on chest radiography.
and management of sepsis. More recent data bring
It has to be made clear from the outset that ARDS
the reported declines into question, and suggest that
is not a disease. It is a state of dramatically diminished
ARDS occurs in 10.4% of all ICU admissions, with a
lung function of variable aetiology. A working defini-
hospital mortality of 34.9–46.1%, although these data
tion of ARDS was established in 1994 by the American-
are not without controversy.
European Consensus Conference. A more recent report
Once treatment of the precipitating condition has
recommends use of definitions of mild, moderate and
commenced, prognostic factors relate to the patient’s
severe ARDS, based on the degree of hypoxaemia
response to therapy. Severe arterial hypoxaemia
(Table 44.1). Additionally, the exclusion of pulmo-
(PaO2/FiO2 < 100 mmHg) and an increase in the pul-
nary oedema secondary to cardiac failure is now not
monary dead-space fraction (>0.60) are associated
mandated, positive end expiratory pressure (PEEP) is
with increased mortality. Mortality also correlates
accounted for as an indicator of severity, and a known
with the number of organ system failures, increasing
ARDS risk factor must be present within 7 days of onset.
to 83% when three or more are present. Complications
ARDS develops after exposure to a wide variety
appearing during the course of ARDS, including cir-
of insults, and given the nature of the diagnostic cri-
culatory shock, acute renal failure and liver dysfunc-
teria, should be considered a syndrome rather than
tion, allied with age over 60 years, are associated with
a disease. Initiating insults can be divided into two
a higher mortality. Lung function in most survivors
groups: direct (e.g. pneumonia) or indirect (e.g. sep-
returns to normal over 6–12 months, although the
sis) as outlined in Table 44.2. Risk of progression to
majority have persistent, abnormal exercise endur-
ARDS varies according to the type, number and sever-
ance, and neuromuscular and neurocognitive mor-
ity of predisposing conditions, as well as the genetics
bidity significantly impairs longer term health related
and other patient characteristics including gender,
quality of life.
body mass index, smoking status, and alcohol usage.
Diagnosing and treating conditions that mimic, or are
associated with, ARDS is the first principle of success- Pathobiology
ful management; prediction scores such as the Lung
Injury Protection Score (LIPS) are intended to facili- Alveolar Epithelial Injury
tate early recognition and treatment. The alveolar epithelium is composed of approxi-
mately equal numbers of flat type I cells (hAT1) and
Incidence and Outcomes cuboidal type II cells (hAT2). hAT2 have several criti-
Data from the late 1990s determined that the age cal functions, including surfactant production, ion
adjusted incidence of ARDS was 86.2 per 100,000 transport and functioning as progenitor cells for the
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Section 7: Disease Management
Table 44.1 Berlin definition of ARDS
Mild ARDS Moderate ARDS Severe ARDS

Timing Within 1 week of a known clinical insult or new or
worsening respiratory symptoms
PaO2:FiO2 201–300 mmHg ≤200 mmHg ≤100 mmHg
PEEP PEEP ≥ 5 cmH20 PEEP ≥ 5 cmH20 PEEP ≥ 10 cmH20
Chest X-ray Bilateral opacities Bilateral opacities Bilateral opacities
PaO2/FiO2 arterial partial pressure of oxygen/inspired oxygen fraction.

PEEP positive end expiratory pressure.
Table 44.2 Hallmarks of indirect versus direct ARDS
Indirect ARDS Direct ARDS

Causes Severe sepsis Pneumonia
Trauma Aspiration
Blood product transfusion Smoke inhalation
Pancreatitis Pulmonary contusion
Cardiopulmonary bypass Reperfusion injury
Burns
Clinicopathological Neutrophilic alveolitis Neutrophilic alveolitis
hallmarks Hyaline membranes Hyaline membranes
Microthrombi Microthrombi
Predominance of endothelial injury Predominance of alveolar epithelial injury
Imaging/plasma evidence of (non-pulmonary) Thoracic imaging evidence of initiating pulmonary
pathology, e.g. pancreatitis pathology, e.g. lung contusion
regeneration of hAT1 cells after injury. Typical histo- the expression of leucocyte adhesion molecules, and
logical appearances of ARDS include extensive necro- cell–cell interactions with resident lung cells, particu-
sis of hAT1 and the formation of protein-rich hyaline larly alveolar macrophages.
membranes on a denuded basement membrane. The
extent of alveolar epithelial damage is a predictor of Endothelial Activation and Injury
outcome. The pulmonary endothelium forms a continuous
Alveolar fluid clearance by hAT2 is primarily barrier of endothelial cells, which regulate fluid per-
driven through sodium uptake on the apical mem- meability as well as modulating host inflammation,
brane, followed by extrusion of sodium on the baso- vascular tone, angiogenesis and interactions with
lateral surface by Na+K+- ATPase. Loss of alveolar blood-borne cells. Loss of barrier integrity, character-
epithelial integrity and down regulation of sodium ised by the formation of reversible intercellular gaps
and chloride transporters results in the accumulation between endothelial cells, is accepted as the ultras-
of protein-rich and highly cellular oedema fluid in the tructural basis for the pulmonary oedema observed
interstitium and alveoli. Loss of surfactant producing in ARDS. Gap formation is induced by the binding of
hAT2, allied with the effect of plasma proteins in the mediators, including thrombin and tumour necrosis
airspace, contributes to ARDS through atelectasis, factor-alpha (TNF), which induce cytoskeletal rear-
increased oedema formation and impairment of local rangement and endothelial barrier disruption.
host defence. Clinically this presents with collapse Similar to the alveolar epithelium, the lung
of lung units and reduced pulmonary compliance. endothelium orchestrates and propagates the inflam-
Epithelial cells also play key roles in regulating the matory response. Endothelial cells release cytokines
inflammatory response through production of injury- and chemokines, up regulate the expression of adhe-
driven pro-inflammatory cytokines and chemokines, sion molecules, and shift from an antithrombotic to
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Chapter 44: Respiratory Disorders: ARDS
a pro-thrombotic activated state, resulting in capil- Monocytes appear to play a role in regulating
lary thrombosis and extravascular fibrin deposition, neutrophil influx to the lung. However, whilst direct
potentiating pulmonary inflammation and contribut- depletion of monocytes in mice consistently reduced
ing to the increased dead-space fraction observed in LPS-induced blood and alveolar neutrophilia, as well
ARDS. Inflammation in the vascular space also coun- as lung injury, peripheral mononuclear cell depletion
teracts hypoxic pulmonary vasoconstriction, partly by in humans was unsuccessful in preventing the recruit-
causing dysregulation of the production of vasoactive ment of neutrophils into the alveolar space.
mediators including prostanoids, endothelins and
nitric oxide. Ventilator Associated Lung Injury
The application of mechanical ventilation exacer-
Role of Circulating Cells bates ARDS in a process called ventilator-associated
The recruitment of circulating inflammatory cells lung injury (VALI). Mechanical forces applied during
into the lung has long been recognised in ARDS. ventilation cause physical disruption of the alveolar-
Neutrophils are central to the initiation and propaga- capillary membrane leading to pulmonary oedema,
tion of the inflammation observed, and neutrophilic whilst cyclical stretch induces activation of cell-
alveolitis is a histological hallmark of ARDS (see signalling pathways in epithelial, endothelial and

Figure 44.1). The extent of neutrophilia present within inflammatory cells. In the context of the already
the bronchoalveolar lavage fluid (BALF) of patients injured lung, this results in pro-inflammatory and/or
with ARDS has been reported to correlate with clinical pro-fibrotic responses both locally and in the systemic
outcome. However, the presence of neutrophils per se circulation. Thus, in addition to local injury, VALI
is not damaging, rather the priming/activation status can drive systemic inflammation and extrapulmonary
of these cells is the major determinant of their sub- organ damage. This is reflected in the observation that
sequent injury-inducing behaviour. Recent data have the majority of patients with ARDS die from multisys-
shown that the healthy human pulmonary endothe- tem organ failure, rather than hypoxaemic respiratory
lium plays a role in host defence by trapping primed/ failure.
activated neutrophils, facilitating their d
epriming, and
later releasing them back into the systemic circulation Resolution of Inflammation and Repair of
in a quiescent state. Failure of this homeostatic deprim-
ing mechanism was observed in patients with ARDS.
the Injured Lung
Most patients gradually recover normal physiology
and lung function. In the alveolar epithelium, hAT2
cells proliferate in response to stimulation by epithe-
lial growth factors. hAT2 cells are thought to act as
progenitor cells for both daughter type II cells and
type I cells. Local and bone marrow derived stem cells
may also contribute to repair. Resolution of inflam-
mation is macrophage and T-cell driven. Collectively,
these mechanisms combine to reconstitute the epithe-
lial barrier and restore lung function.
If epithelial injury is severe, or repair is impaired,
a fibroproliferative phase of ARDS can ensue either
following, or in parallel with, epithelial injury. During
this phase, mesenchymal cells proliferate, neovas-
cularisation occurs, and the alveolar space becomes
filled with activated fibroblasts and myofibroblasts
Figure 44.1 Bronchoalveolar lavage fluid from a patient with that synthesise excessive collagenous extracellular
ARDS. Photomicrograph of modified Wright’s stained cytospin.
The white arrow denotes a hypersegmented neutrophil; the black matrix. A small proportion of patients progress to a
arrow denotes a neutrophil which has been efferocytosed by a chronic phase of respiratory insufficiency character-
macrophage. (A black and white version of this figure will appear ised by widespread pulmonary fibrosis, with disor-
in some formats. For the colour version, please refer to the plate
section.) dered lung architecture.
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Clinical Investigations Recruitment manoeuvres involving a transient

increase in transpulmonary pressure are designed
The main clinical priority is identification and treat-
to promote reinflation of collapsed alveoli. A variety
ment of the initiating pathology and any complications
of techniques have been proposed, including graded
that may have ensued. It may be necessary, particu-
incremental pressure increases, and a sustained high
larly in the immune compromised host, to undertake
inflation pressure manoeuvre followed by a decremen-
invasive diagnostic procedures, such as bronchoscopy,
tal reduction to an optimal PEEP level determined
to establish a diagnosis. Further, it has been shown
by dynamic analysis of flow-volume relationships, as
that intercurrent pulmonary infection occurs in up to
well as image guided strategies. Whilst data support
70% of patients with ARDS, necessitating vigilance for
improvements in oxygenation, such manoeuvres are
the subsequent development of infection.
associated with complications, in particular haemo-
dynamic compromise, barotrauma and exacerbation
Ventilator Management of existing air leaks; these appear to relate to the fre-
quency of applied manoeuvres.
Protective Ventilation
The magnitude of the clinical burden of VALI was
demonstrated by the ARDS Network study, in which Ventilatory Modes
patients with ARDS were randomised to receive either Despite inverse ratio ventilation (IRV) demonstrating
a high tidal volume (12 ml/kg predicted body weight no clear benefit when compared with conventional
(PBW)) with end inspiratory pressure limited to a pla- ventilator modes, the application of airway pressure
teau pressure Pplat ≤ 50 cmH2O, or a low tidal volume release ventilation (APRV) in ARDS has been advo-
(6 ml/kg PBW) and Pplat ≤ 30 cmH2O. A PEEP ladder cated by some centres. APRV utilises inverse ratio,
was used to determine the PEEP level administered, pressure controlled, intermittent mandatory ventila-
according to the fraction of inspired oxygen and the tion in patients with unrestricted spontaneous breath-
respiratory rate. The low tidal volume cohort demon- ing to maintain alveolar recruitment and improve
strated a 9% absolute reduction in mortality (40% to oxygenation, whilst limiting inflation pressures and
31%). Accordingly, low tidal volume ventilation has sedation. Unlike IRV, APRV does not mandate paral-
become the standard of care in ARDS, and the goal ysis and hence is an attractive mode. Nonetheless,
of mechanical ventilation has shifted from normalisa- APRV risks tidal hyper-inflation, increased transpul-
tion of gas exchange parameters to minimising VALI monary pressures, and has shown no clear benefit
with pragmatic acceptance of modest biochemical over conventional modes. The use of high-frequency
derangement. oscillatory ventilation (HFOV) to deliver small tidal
volumes at high frequency with high mean airway
High PEEP and Recruitment Manoeuvres pressures has been similarly tempered by two large
multicentre trials demonstrating no benefit in one and
The application of PEEP has been used to mitigate
increased mortality in the other. Accordingly, despite
the pulmonary oedema and atelectasis of ARDS.
the theoretical mitigation of VALI, HFOV can no
Several studies have failed to show clinical benefit
longer be recommended in ARDS, and conventional
of higher PEEP levels; nonetheless, a meta- analy-
ventilator modes should suffice for the majority of
sis demonstrated improved survival in those with
patients. Where conventional modes fail to facilitate
most severe physiological derangements (PaO2:FiO2
low tidal volume ventilation and acceptable physiol-
< 200 mmHg). Despite these data, consensus for this
ogy, extracorporeal gas exchange techniques should
approach is lacking, particularly as response is hetero-
be considered in appropriate patients.
geneous and may be associated with lung hyperinfla-
tion and haemodynamic compromise. Determination
of ‘optimal PEEP’ levels has thus far been elusive; cal- Extracorporeal Gas Exchange
culation of driving pressure, estimation of transpul- Extracorporeal gas exchange (ECGE) is technol-
monary pressures using an oesophageal probe and ogy whereby blood is drained from a major vein,
imaging techniques have shown promise but none pumped through an artificial membrane to facilitate
have been assessed in prospective trials and cannot be gas exchange, and returned to the venous or arterial
recommended routinely. system, depending on the physiological needs of the
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369
patient. Various extracorporeal circuit arrangements patients treated after day 13. In addition, a significant
are available and are discussed in Chapter 24. proportion of patients required re- ventilation fol-
lowing steroid weaning, and concerns persist about
Non-ventilator Therapies the relationship between steroid therapy and ICU-
acquired weakness.
General Supportive Measures Inhaled vasodilators, including nitric oxide, pros-
tacyclin and prostaglandin E1, improve ventilation-
Prompt administration of appropriate antibiotics in
perfusion matching and pulmonary hypertension
sepsis, a reduction in iatrogenic injury through use
by inducing selective vasodilation in well-ventilated
of reduced tidal volume ventilation and stewardship
lung. Transient improvements in oxygenation are well
for hospital-acquired aspiration/ventilator-associated
established, but inhaled vasodilators are expensive,
pneumonia, coupled with lower blood transfusion
challenging to administer and associated with adverse
thresholds and the removal of females from the plasma
events without concomitant mortality benefit. Their
donor pool have combined to limit hospital-acquired
use should therefore be limited to those patients with
ARDS. The use of sedation holds, spontaneous breath-
refractory hypoxaemia, either as a bridge to extra-
ing trials and early mobilisation/rehabilitation pro-
corporeal oxygenation, or to provide time for ancil-
grammes, where appropriate, are also likely to have
lary therapies to take effect, or for those patients with
contributed.
reversible pulmonary hypertension in the setting
Non-hydrostatic pulmonary oedema in the con-
of ARDS.
text of increased pulmonary vascular permeability is
Neuromuscular blockade is used in over half of
pathogonomic of ARDS. Limitation of fluid adminis-
ARDS patients to prevent ventilator dysynchrony.
tration is therefore an attractive strategy. Studies have
A recent randomised controlled trial found the early
shown an association between a persistent positive
use (<48 hours of ARDS onset) of cisatracurium
fluid balance and poor outcome in ARDS. The latter
improved 90-day survival in those patients with a
hypothesis is supported by a study assessing the safety
PaO2:FiO2 ≤ 150 mmHg. Of note, neuromuscular
and efficacy of ‘conservative’ versus ‘liberal’ fluid man-
weakness was not more prevalent in the cisatracurium
agement strategies. Although the primary endpoint
group. Further trials are required to clarify whether
(death at 60 days) did not differ between strategies,
these effects are reproducible and to clarify the mech-
benefits in ventilator free and organ failure free days
anisms of benefit.
were observed in the ‘conservative’ group, without an
Despite promising experimental data, recent large
increase in renal dysfunction.
trials of a range of therapies, the majority of which
Wherever possible, supplemental feeding should
were designed to reduce cellular and mediator driven
be administered via the enteral route. The use of pro-
inflammation, have failed to demonstrate improve-
kinetic drugs where needed, and the avoidance of
ments in clinical outcomes. Statins, beta-2-agonists,
agents that delay gastric emptying, may limit the risk
ketoconazole, vitamin D supplementation and anti-
of aspiration pneumonitis.
oxidants were all found not to confer benefit. This has
highlighted the need to limit the heterogeneity of sub-
Pharmacotherapy jects recruited into clinical trials through improved
The anti- inflammatory and antifibrotic properties understanding of the pathobiology.
of steroids present a rational therapy to dampen the
dysregulated inflammation which propagates ARDS.
Numerous studies have failed to demonstrate clinical Cell Therapies
benefit from a short course of high dose steroids for Several clinical trials of mesenchymal stem cells (MSCs)
the prevention, or treatment, of early ARDS (within for the treatment of ARDS are currently underway
72 hours of onset), with some suggesting steroids may (ClinicalTrials.gov: NCT01775774, NCT02444455,
be harmful. The role of steroid therapy in late or unre- NCT02215811, NCT02611609). However, engraftment
solving ARDS, i.e. ≥7 days, remains controversial, within the lung does not seem to be the major thera-
with data suggesting improvements in both mortal- peutic effect of MSCs, rather the effect derives from
ity and liberation from mechanical ventilation, but their capacity to secrete paracrine factors that modulate
post hoc analysis indicating an increased mortality in immune responses and alter the host responses to injury.
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Pre-clinical work has shown that cryopreserved alloge-

neic human MSCs are therapeutic in a human ex vivo
Further Reading
lung model, but the antimicrobial effects of the MSCs Bellani G, Laffey JG, Pham T, et al. Epidemiology,
patterns of care, and mortality for patients with acute
could be largely duplicated by keratinocyte growth fac-
respiratory distress syndrome in intensive care units
tor (KGF), a major paracrine product of MSCs. A clini- in 50 countries. Journal of the American Medical
cal trial investigating the efficacy and safety of KGF in Association. 2016; 315: 788–800.
ARDS has been completed, but the results have not as Bernard GR, Artigas A, Brigham KL, et al. The
yet been reported (ISRCTN95690673). American–European Consensus Conference on
ARDS: definitions, relevant outcomes, and clinical
trial coordination. American Journal of Respiratory and
Prone Positioning Critical Care Medicine. 1994; 149: 818–824.
Mechanical ventilation in the prone position is Boyle AJ, MacSweeney R, McAuley DF. Pharmacological
frequently used in the management of refrac- treatments in ARDS: a state-of-the-art update. BMC
tory hypoxaemia in ARDS. Approximately 60% of Medicine. 2013; 11: 166.
patients demonstrate improvements in oxygena- Ferguson ND, Cook DJ, Guyatt GH, et al. High-frequency
tion, which are often sustained on return to the oscillation in early acute respiratory distress syndrome.
supine position. Proposed mechanisms of benefit New England Journal of Medicine. 2013; 368: 795–805.
include more homogenous distribution of ventila- Guérin C, Reignier J, Richard J-C, et al. Prone positioning
tion, better ventilation-perfusion matching and a in severe acute respiratory distress syndrome. New
England Journal of Medicine. 2013; 368: 2159–2168.
reduction in VALI. Recently, proning, combined
with a protective ventilatory strategy, for at least 16 Herridge MS, Tansey CM, Matte A, et al. Functional
disability 5 years after acute respiratory distress
hours a day in patients with severe ARDS (PaO2/
syndrome. New England Journal of Medicine. 2011;
FiO2 < 150 mmHg with PEEP of at least 5 mmHg 364: 1293–1304.
and FiO2 of ≥0.6) demonstrated a significant reduc-
Lee JW, Krasnodembskaya A, McKenna DH, et al.
tion in both 28-day and 90-day mortality. Whilst Therapeutic effects of human mesenchymal stem cells
proning confers a risk of pressure ulcers, facial in ex vivo human lungs injured with live bacteria.
oedema and endotracheal tube obstruction/ dis- American Journal of Respiratory and Critical Care
placement, favourable haemodynamic effects have Medicine. 2013; 187: 751–760.
been observed with increasing cardiac index in Marshall RP, Webb S, Hill MR, et al. Genetic
those patients with preload reserve. polymorphisms associated with susceptibility and
outcome in ARDS. Chest. 2002; 121: 68S-69S.
Miller F, Summers C, Griffiths M, et al. The pulmonary
Learning Points endothelium in acute respiratory distress
syndrome: insights and therapeutic opportunities.
• ARDS is a heterogeneous syndrome rather than Thorax. 2016; 71: 462–473.
a single disease, hence a variety of supportive National Heart Lung and Blood Institute (NHLBI)
and therapeutic approaches may be required for Acute Respiratory Distress Syndrome Clinical Trials
optimal management. Network. Comparison of two fluid-management
• The mainstay of ARDS management is the strategies in acute lung injury. New England Journal of
identification and treatment of the predisposing Medicine. 2006; 354: 2564–2575.
condition, along with supportive care, which NHLBI Acute Respiratory Distress Syndrome Network.
includes lung-protective ventilation. Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and
• Fluid restriction, after patients are appropriately
the acute respiratory distress syndrome. New England
resuscitated. Journal of Medicine. 2000; 342: 1301–1308.
• The early, and short-term, use of cisatracurium
Papazian L, Forel J-M, Gacouin A, et al. Neuromuscular
in more severe ARDS cases may improve blockers in early acute respiratory distress
outcome over and above lung-protective syndrome. New England Journal of Medicine. 2010;
ventilation. 363: 1107–1116.
• There are currently no licensed pharmacological Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and
therapies for ARDS. economic assessment of conventional ventilatory
16:16:50
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supprt versus extracorporeal membrane oxygenation Summers C, Singh NR, White JF, et al. Pulmonary
for severe adult respiratory failure (CESAR): a retention of primed neutrophils: a novel protective
multicentre randomised controlled trial. Lancet. 2009; host response, which is impaired in the acute
374: 1351–1363. respiratory distress syndrome. Thorax. 2014;
Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute 69: 623–629.
respiratory distress syndrome: the Berlin definition. Villar J, Schultz MJ, Kacmarek RM. The LUNG SAFE: a
Journal of the American Medical Association. 2012; biased presentation of the prevalence of ARDS! Critical
307: 2526–2533. Care. 2016; 20: 108.
MCQs
1. ARDS is defined by the following except: (d) Liberal administration of intravenous fluids to
(a) Arterial hypoxaemia ensure adequate tissue perfusion
(b) Hypercapnoea (e) Daily recruitment manoeuvres
(c) Bilateral pulmonary infiltrates on chest radiograph 4. Regarding ECMO:
(d) Progressive dyspnoea over 4 weeks (a) It has demonstrated a clear mortality benefit in
multiple clinical trials in ARDS
(e) Histological evidence of diffuse alveolar damage
(b) Provides just oxygenation with no carbon dioxide
2. The following have demonstrated a mortality benefit removal
in ARDS:
(c) Has a complication rate <5%
(a) Inhaled nitric oxide
(d) Should be considered in patients who deteriorate
(b) Cisatracurium despite optimal medical therapy and 4 weeks of
(c) Ketoconazole supportive ventilation
(d) Surfactant therapy (e) Facilitates protective lung ventilator strategies
(e) Mesenchymal stem cell therapy 5. Evidence-based mechanical ventilation in ARDS
includes:
3. ARDS management includes:
(a) Low tidal volume (6 ml/kg PBW) ventilation
(a) Transfusion to >11 g/dl haemoglobin concentration
to optimise tissue oxygen delivery (b) High frequency oscillatory ventilation (HFOV)
(b) Administration of beta-2-agonists to improve (c) Airway pressure release ventilation (APRV)
alveolar fluid clearance (d) Inversed I:E ratio ventilation
(c) Early appropriate antibiotics in the management of (e) Utilisation of PEEP >10 in all cases
sepsis related ARDS
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Section 7
Chapter
Cardiovascular Disorders: the Heart Failure
45 Patient in the Intensive Care Unit

Anna Kydd and Jayan Parameshwar
Introduction Bedside assessment may provide clues to the haemo-

dynamic profile of a patient. It is important to dis-
The combination of the aging of the population and
tinguish between elevated and non-elevated cardiac
improved survival after myocardial infarction has
filling pressures (‘wet’ or ‘dry’), and adequate or
increased the prevalence of heart failure. Most patients
severely impaired tissue perfusion (‘warm’ or ‘cold’)
with advanced heart failure are admitted to hospital
(see Figure 45.1).
as a result of acute decompensation but some patients
Elevated filling pressure can be diagnosed clini-
with new onset heart failure may present acutely in
cally by orthopnoea or by elevated jugular venous
extremis. Patients with impaired ventricular function
pressure. Blood pressure is only a guide to tissue per-
who undergo surgery may also present with low out-
fusion; proportional pulse pressure (pulse pressure/
put states in the ICU.
systolic pressure) less than 25% has been reported
The clinical syndrome of heart failure can result
to correlate with a cardiac index less than 2.2 l/min/
from any structural or functional impairment of ven-
m2 in the population of patients referred for cardiac
tricular filling or ejection of blood. Coronary artery
transplantation.
disease remains the most common cause of heart
Patients admitted to the critical care unit are most
failure. In younger patients (such as the population
likely to have elevated filling pressures and inadequate
referred for cardiac transplantation), dilated cardio-
end-organ perfusion (wet and cold). This group is
myopathy (often of unknown aetiology) is the com-
associated with the highest mortality.
monest cause. The true incidence of acute myocarditis
in patients with a short history of heart failure is not
known because of the difficulty in confirming the Cardiorenal Syndrome
diagnosis. Both an acute deterioration and chronic impairment
of cardiac function can lead to a progressive decline
in renal function. The umbrella term cardiorenal syn-
Clinical Presentation drome is used to describe this. The pathophysiology
Patients requiring admission to critical care because varies depending on specific clinical circumstances;
of severe heart failure usually have one of two clinical however it involves transrenal perfusion pressure,
syndromes: intrarenal haemodynamics and systemic neurohor-
1. Pulmonary oedema accompanied by severe monal factors. Alterations in the balance of vasocon-
respiratory distress and low oxygen saturation strictor and vasodilator hormones adversely affect
(prior to treatment). renal function, and the combination of increased cen-
2. Cardiogenic shock: defined as tissue tral venous pressure with low systemic pressure may
hypoperfusion induced by heart failure after lead to a severe compromise of net renal perfusion
correction of preload. It is usually characterised pressure.
by hypotension (systolic BP <90 mmHg), oliguria In the acute setting, worsening renal function
(<0.5 ml/kg/hour) and evidence of end-organ (acute kidney injury) frequently complicates hospital
dysfunction such as renal, hepatic and cognitive admissions with acute decompensated heart failure.
impairment, and elevated blood lactate level. Patients with worsening renal function have a higher
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373
Chapter 45: Cardiovascular Disorders: Heart Failure
Signs/symptoms of congestion Figure 45.1 Assessment of

(elevated filling pressures) haemodynamic profile using
haemodynamic signs and
Orthopnoea
symptoms of patients presenting
High JVP with heart failure. JVP jugular
Peripheral oedema venous pressure.
Pulmonary oedema
Ascites
S3 or gallop rhythm
No Yes
Evidence of hypoperfusion Warm & Dry Warm & Wet

Cold extremities No PCWP normal PCWP high
Hypotension CI normal CI normal
Renal dysfuction
Altered mental status
Hepatic dysfunction
Narrow pulse pressure Cold & Dry Cold & Wet
Hyponatremia Yes PCWP low/normal PCWP low/normal
CI normal CI reduced
mortality and morbidity and increased duration of pulmonary artery systolic pressure may also be
hospitalisation. estimated from the tricuspid regurgitation jet and
In the more chronic state, renal dysfunction devel- echocardiography.
ops in patients who have chronic volume overload, 4. Blood tests: full blood count, coagulation screen,
prior renal dysfunction, right ventricular dysfunction C-reactive protein, creatinine and electrolytes,
and high baseline diuretic requirements. When filling glucose and liver function tests in all patients.
pressures are measured they exceed the optimal levels Troponin and plasma BNP (B-type natriuretic
required to maintain cardiac output. A stable clinical peptide) may also be indicated. For the assessment
state may be maintained in some patients with high of a patient presenting with acute dyspnoea a low
serum urea and creatinine levels but the prognosis is BNP has a high negative predictive value for heart
poor. Inotropic infusions may relieve the congestion failure as the aetiology. BNP may be less helpful in
and improve renal function but the problem often the critical care setting.
recurs when inotropes are withdrawn. 5. Coronary angiography if revascularisation is
indicated.
Investigations
In addition to a detailed clinical history and physical Monitoring
examination a number of investigations are required: 1. Non-invasive monitoring – temperature,
1. Electrocardiogram to determine rhythm and respiratory rate, blood pressure, continuous ECG
aetiology of heart failure (e.g. acute coronary monitoring and pulse oximetry are required for all
syndrome or myocarditis). patients.
2. Chest radiograph for heart size, pulmonary 2. Arterial line –essential in unstable patients for
congestion, lung consolidation or pleural continuous arterial blood pressure monitoring
effusions. and frequent analysis of blood gases.
3. Echocardiography to assess regional and global 3. Central venous line –monitoring right sided
left and right ventricular function, valve structure filling pressure is often essential in patients with
and function, pericardial effusion, and mechanical advanced heart failure and a central venous line
complications of myocardial infarction. The is required for the delivery of fluids and drugs.
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374
Estimation of superior vena caval or right atrial the circulation and is a powerful predictor of
oxygen saturation can be a useful marker of prognosis in cardiogenic shock. It is calculated
oxygen transport. Central venous pressure may be as the product of simultaneous mean arterial
significantly affected by positive end-expiratory pressure (MAP) and cardiac output corrected
pressure ventilation. for a constant and expressed as watts.
• Pulmonary artery catheter (PAC) –PAC allows • Although PAC is the ‘gold standard’ there
direct measurement of right atrial (RA), right are a number of non-invasive cardiac output
ventricular (RV), pulmonary artery (PA), monitoring devices available that can derive
pulmonary capillary wedge pressure (PCWP) haemodynamic data, but most have not been
and calculation of pulmonary and systemic validated in low cardiac output states.
vascular resistance. Mixed venous oxygen 4. Echocardiography –there is an emerging role
saturation can also be monitored. This is for both transthoracic and transoesophageal
particularly useful in the presence of severe echocardiography in monitoring
tricuspid regurgitation when the cardiac output haemodynamics in critically ill patients;
derived by thermodilution may be inaccurate. however, interpretation of data requires specific
• In patients with heart failure, right atrial training and expertise.
pressure does not correlate well with left
sided filling pressure. In many situations, an Treatment
estimate of left atrial pressure is invaluable. The treatment of chronic heart failure has been the
In patients with a high pulmonary vascular subject of several large randomised clinical trials and
resistance (PVR) associated with heart failure, evidence-based guidelines are available.
direct measurement of pulmonary pressure Critically ill patients with acute heart failure are
is important. In patients requiring inotropic a heterogeneous group with respect to aetiology,
or vasoconstrictor drugs, monitoring of haemodynamic abnormalities and comorbidities, and
cardiac output and estimation of systemic are therefore difficult to subject to randomised trials.
vascular resistance facilitates therapy based on Treatment strategies should be based on the underly-
pathophysiological principles. ing pathophysiology with the aim of reversing haemo-
• Complications associated with the use of a PAC dynamic abnormalities. If an underlying treatable
increase with duration of use and it should cause is identified, clinical condition should be opti-
not be left in situ longer than necessary. In mised so that definitive treatment can be carried out
advanced heart failure, therapy tailored to with the minimum of risk. Immediate therapy should
haemodynamic goals as guided by PAC has focus on relieving symptoms. Reducing congestion
been shown to result in sustained improvement is often the most effective way of achieving this (see
in symptoms, stroke volume and cardiac Table 45.1).
output. General management involves a multidiscipli-
• Cardiac power output (CPO) describes the nary team due to the complexity of the pathophysi-
relationship between flow and pressure in ology in the critically ill heart failure patient. In
Table 45.1 Treatment goals in advanced heart failure

Clinical Elimination of peripheral and pulmonary oedema
Systolic blood pressure >85 mmHg
Stable or improving renal function
Normal or improving liver function and coagulation parameters
Adequate oxygenation
Haemodynamic Central venous/right atrial pressure ≤8 mmHg
Pulmonary capillary wedge pressure ≤16 mmHg
Cardiac index >2 l/min/m2
Mixed venous oxygen saturation >60%
Systemic vascular resistance 800–1200 dyne s cm−5 (secondary goal to guide therapy)
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375
addition to the specific treatments described below, Patients with acute decompensation of chronic heart
management should include investigation and cor- failure are likely to be on diuretic therapy when admit-
rection of anaemia, electrolyte abnormalities, thy- ted. Data are lacking on the relative efficacy and tol-
roid and adrenal function and optimal glucose erability of different diuretics. In the acute setting, a
control. Infection is common; therefore standard loop diuretic is administered intravenously with dose
infection control measures and evidence-based anti- titration to produce optimal urine output. A large
microbial treatment are essential. Patients should bolus of diuretic may also lead to reflex renal vaso-
receive appropriate nutrition, mobilisation and constriction and a higher risk of ototoxicity. An intra-
physiotherapy. Provision of psychological support venous infusion of furosemide at 5–10 mg/hour is
and involvement of palliative care teams are also sufficient in most patients once steps have been taken
important considerations. to increase the cardiac output. Fluid restriction (usu-
ally to 1.5 l/day) is an important adjunct to diuretic
therapy in severely fluid-overloaded patients. Using
Oxygenation a ‘fluid challenge’ in such patients with obvious fluid
Achieving an adequate level of oxygenation at the cel- retention is irrational and has no place in treatment
lular level is important to prevent end-organ dysfunc- of heart failure patients in the cardiothoracic ICU;
tion. Treatment should aim to achieve optimal rather inadequate urine output in these patients is usually
than supraphysiological arterial oxygenation, i.e. arte- related to a low cardiac output and treating this often
rial oxygen saturation above 95%. Respiratory muscle requires inotropic therapy. Once filling pressures have
fatigue often results from hypoxaemia and low cardiac been reduced to normal, the dose of diuretic should be
output. reduced; the dose required to maintain euvolaemia is
usually less than that required to achieve it.
Non-invasive Ventilation The combination of a thiazide (e.g. metolazone or
Either continuous positive airway pressure (CPAP) or bendroflumethiazide) with a loop diuretic can aug-
non-invasive ventilation (NIV) can be used to reduce ment the diuresis achieved in patients with chronic
the work of breathing. Both CPAP and NIV result heart failure and is of use in the acute setting. Heart
in pulmonary recruitment and an increase in func- failure patients are often hyponatraemic in the ICU
tional residual capacity and a reduction in pulmonary and care needs to be taken not to exacerbate this
oedema. Clinical trials comparing CPAP with stand- with combination diuretic therapy. Serum potassium
ard therapy have shown a decreased need for endotra- should be monitored as hypokalaemia may predispose
cheal intubation. to arrhythmias. Combining loop diuretics with a min-
eralocorticoid receptor antagonist like spironolactone
or eplerenone may be effective provided the serum
Mechanical Ventilation with Endotracheal potassium is <5 mmol/l and serum creatinine <200
Intubation µmol/l.
If non-invasive ventilation does not reverse hypox-
aemia or if there is compromise to airway patency, Vasodilators
endotracheal intubation is indicated. In the absence of severe hypotension, vasodilators are
indicated in most patients with acute heart failure.
Drug Therapy Decreasing preload relieves congestion and decreas-
The major goals of medical therapy in the heart failure ing afterload is usually beneficial as most patients with
patient in the ICU are (i) reducing venous congestion heart failure are vasoconstricted (Table 45.2). When
(optimising preload), (ii) optimising afterload with administering vasodilators or positive inotropic
vasodilators, in the absence of severe hypotension, drugs, the following equation is useful in manipulat-
and (iii) inotropic support. ing the circulation:
MAP − CVP = CO × SVR
Diuretics where MAP is the mean arterial pressure, CVP is the
The reduction of elevated filling pressures is the most central venous pressure, CO is the cardiac output and
effective way to relieve symptoms of heart failure. SVR is the systemic vascular resistance.
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Table 45.2 Typical doses of intravenous inotropes used in worsening renal function, it is reasonable to use this
heart failure combination orally or intravenously.
Drug Bolus Dose
Dopamine No 2–10 μg/kg/min Inotropic Support
Dobutamine No 2–20 μg/kg/min Inotropic agents are indicated in the presence of tissue
Adrenaline No 0.05–0.5 μg/kg/min hypoperfusion and pump failure often manifested by
Noradrenaline No 0.02–0.2 μg/kg/min
worsening renal function or fluid retention (periph-
eral or pulmonary oedema) refractory to treatment
Enoximone 0.25–0.75 mg/kg 1.25–7.5 μg/kg/min
with diuretics and vasodilators. A common clinical
Milrinone 25–75 μg/kg 0.375–0.75 μg/kg/min
scenario is a volume-overloaded patient with hypoten-
Levosimendan 12–24 μg/kg 0.05–0.2 μg/kg/min sion, hyponatraemia, and a rising serum urea and cre-
atinine on intravenous diuretic therapy. Continuing
such therapy is likely to exacerbate metabolic abnor-
Nitrates malities and is unlikely to induce a significant diure-
In low doses, nitrates are venodilators but high doses sis. Intravenous inotropic therapy may be necessary to
can also cause arterial dilatation. They are particu- improve the patient’s haemodynamic state until some
larly useful in acute coronary syndromes associ- form of definitive therapy or long-term palliation can
ated with heart failure. Oral nitrates in combination be considered.
with hydralazine have been shown to be beneficial in Although inotropic agents in heart failure can
chronic heart failure and at least two randomised con- result in short-term beneficial haemodynamic effects,
trolled trials have shown that intravenous nitrate in they increase myocardial oxygen consumption and
combination with furosemide is superior to furosem- carry a risk of inducing life-threatening arrhythmia.
ide alone. Tolerance to nitrate can develop within 24 Rational use of inotropic therapy in a critically ill
hours of commencing an infusion. population requires invasive haemodynamic moni-
toring. The lowest effective dose should be used;
Nesiritide
patients receiving beta-blockers may require higher
Nesiritide (recombinant brain natriuretic peptide) is doses. Very few trials have been conducted in patients
licensed in the USA for the treatment of acute heart with advanced heart failure and there is no definite
failure. It relaxes smooth muscle leading to arterial evidence of the superiority of one agent compared to
and venous dilatation and leads to an increase in car- any other.
diac output without direct positive inotropic effect.
Compared with nitroglycerin, nesiritide has been Dopamine
shown to produce faster relief of dyspnoea and a more Dopamine has complex effects, which vary according
pronounced decrease in pulmonary capillary wedge to dose. Low doses of dopamine (<2 μg/kg/min) are
pressure. Nesiritide has both natriuretic and diuretic thought to act predominantly on peripheral dopa-
effects although up to half of patients with advanced minergic (D1) receptors leading to vasodilatation.
heart failure are reported to be resistant to its natriu- Although controversial, low dose dopamine has been
retic effect. There is no conclusive evidence that nesi- shown to increase renal blood flow. In addition it is
ritide improves renal function; clinical studies have possible that in some patients it may also have an ino-
not demonstrated better clinical outcomes and it may tropic effect.
increase risk of adverse cardiovascular events. The A higher dose of dopamine (>5 μg/kg/min) has
role of nesiritide in the management of heart failure β-
adrenergic effects increasing cardiac output and
remains unclear. α-
adrenergic effects increasing peripheral vascular
resistance and arterial pressure.
Hydralazine
Hydralazine is a potent arteriolar vasodilator. A com- Dobutamine
bination of hydralazine and nitrates has been shown to Dobutamine acts through stimulation of β1 and β2
be beneficial in patients with chronic heart failure. In receptors and is positively inotropic and chrono-
patients who cannot tolerate an angiotensin converting tropic; it may also induce mild arterial vasodilata-
enzyme inhibitor (ACEI) because of hyperkalaemia or tion. High doses of dobutamine (above 10 μg/kg/min)
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cause vasoconstriction but the exact effect at any maintained for 24 hours, but the haemodynamic
given dose varies between patients. Heart rate is gen- effects persist beyond this, probably because of the
erally thought to increase less than with other cat- long half-life of its metabolite. Levosimendan infu-
echolamines, however atrioventricular conduction sions in patients with heart failure have been associ-
is facilitated. The commonly used dose range is 2 to ated with a dose-dependent increase in stroke volume
10 μg/kg/min. and cardiac output, a decline in the pulmonary capil-
lary wedge pressure, a decrease in SVR and PVR, a
Adrenaline slight decrease in blood pressure and a slight increase
This drug has a high affinity for β1, β2 and α-recep- in heart rate. An improvement in symptoms of dysp-
tors causing inotropy, chronotropy, dromotropy and noea and fatigue has been shown in trials comparing
splanchnic hypoperfusion. It is generally infused at a levosimendan with dobutamine. The haemodynamic
rate of 0.05–0.5 μg/kg/min. effects were seen even in the presence of beta-blocker
therapy. Tachycardia and hypotension are side effects
Noradrenaline associated with the use of levosimendan and it is not
This drug is used to increase systemic vascular resist- recommended in patients with a systolic blood pres-
ance (SVR) because of its affinity for α-receptors. The sure below ~85 mmHg.
lowest dose required to increase the SVR (and hence
the blood pressure), and to maintain perfusion of vital
organs, should be used. Septic shock is a common
Angiotensin Converting Enzyme (ACE)
indication for its use; the occasional patient after acute Inhibitors and Angiotensin Receptor
myocardial infarction will present with a low SVR due
to cytokine release and will benefit from noradrena-
Blockers (ARB)
ACE inhibitors were the first drug class shown to
line. Excessive vasoconstriction is associated with a
improve outcome in severe chronic heart failure. ARBs
reduction in cardiac output.
are used as alternatives in patients intolerant of ACEI.
Type III Phosphodiesterase (PDE) Inhibitors They have no role in the early management of unstable
heart failure patients but should be introduced as soon
PDE inhibitors block the breakdown of cyclic-AMP,
as the patient is haemodynamically stable and has
which modulates intracellular calcium handling.
acceptable perfusion and renal function. ACE inhibi-
Enoximone and milrinone are the two agents used
tors decrease renal vascular resistance, increase renal
in clinical practice. They cause marked peripheral
blood flow and promote sodium and water excretion.
vasodilatation and have positive inotropic effects and
However, in patients with a very low cardiac output,
are therefore useful in patients with advanced heart
they may significantly decrease glomerular filtration
failure who have an elevated SVR and a low cardiac
rate. If patients with acute decompensation of chronic
output. Because of their powerful vasodilating effect,
heart failure are admitted to the ICU, it may be neces-
haemodynamic monitoring is recommended when-
sary to discontinue them temporarily.
ever they are used. Both agents have a long elimina-
tion half-life and tend to accumulate if the patient
is oliguric. As their site of action is distal to the β- Beta-Blockers
adrenergic receptor, PDE inhibitors maintain their The role of beta- blockers in the management of
effect in patients who have been treated with beta- chronic heart failure is well established following sev-
blocking drugs. In patients with atrial fibrillation, they eral large trials involving many thousands of patients.
may increase ventricular rate less than dobutamine. In volume- overloaded patients, beta- blockers are
likely to increase the severity of heart failure and are
Levosimendan best avoided. There is no consensus on the manage-
This drug has two main mechanisms of action: Ca2+ ment of a patient receiving beta-blockers for chronic
ion sensitisation of the contractile proteins (positive heart failure admitted to hospital with acute decom-
inotropic effect) and smooth muscle K+ channel open- pensation. Most will require at least a decrease in
ing (peripheral vasodilating effect). There is also a sug- the dose of the drug but in patients requiring (beta-
gestion that levosimendan has a PDE inhibiting effect. agonist) inotropic therapy it is logical to discontinue
Intravenous infusions of levosimendan are usually beta-blockers altogether.
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Anticoagulation The IABP is extremely useful in critically ill

patients with heart failure who can be stabilised until
Patients should receive standard prophylaxis for preven-
definitive therapy can be carried out. In patients
tion of venous thromboembolism and anticoagulation
requiring support beyond that provided by IABP, con-
for established indications, for example acute coronary
sideration should be given to the use of mechanical
syndromes, pulmonary embolism and atrial fibrilla-
circulatory support. There is no evidence of improved
tion. Patients with evidence of ventricular thrombus on
survival with any form of short-term mechanical sup-
echocardiography should also receive anticoagulation.
port, including IABP, in patients with cardiogenic
Care is needed as concomitant liver dysfunction may
shock. However these therapies may improve haemo-
lead to a prolonged prothrombin time. In patients with
dynamics and get the patient fit for definitive treat-
a creatinine clearance below 30 ml/min, low molecu-
ment (implantable device or heart transplantation).
lar weight heparin in therapeutic doses should be used
cautiously, probably with monitoring of factor Xa level.
Conclusion
Ultrafiltration Advanced heart failure in patients on critical care
units carries a high mortality. Optimal management
Patients with gross fluid retention and hyponatraemia
requires close cooperation between a cardiologist with
present a difficult clinical problem. Diuretics often
an interest in heart failure, an intensive care physi-
worsen hyponatraemia and sometimes features of the
cian and a cardiac surgeon. With appropriate therapy,
cardiorenal syndrome become apparent. Inotropic
many critically ill patients can be resuscitated and
drugs may help in this situation but if therapy needs
returned to a productive life.
to be prolonged, the risk of arrhythmia needs to be
considered. Continuous venovenous haemofiltration
(CVVH) is effective in removing fluid and the rate of Learning Points
fluid removal can be tailored to the patient’s needs. • Heart failure is most commonly secondary to
CVVH may also remove cytokines with myocardial coronary artery disease and carries a poor overall
depressant properties (e.g. tumour necrosis factor) as prognosis.
macromolecules up to 20,000 Da can pass through the
• Admission to critical care is usually due to
ultrafiltration membrane. If necessary, large volumes
pulmonary oedema or cardiogenic shock.
of fluid can be removed in a relatively short time to
• The major goals of medical therapy for the heart
get the patient ready for a definitive procedure (heart
failure patient in the ICU are (i) optimising
transplantation, mechanical circulatory support).
preload, (ii) optimising afterload and (iii)
CVVH usually requires large-bore central venous
increasing cardiac output with inotropic support
access although there are devices to allow ultrafiltra-
when required.
tion via cannulae in peripheral arm veins. Although
the maximum rate of fluid removal is less than that • Aggressive diuresis may be needed, and renal
attainable by central CVVH, an adequate rate is replacement therapy may be necessary to remove
achieved for the most common clinical situations. an adequate amount of fluid.
Compared to high dose diuretic therapy, ultrafil- • Inotropes are often started to enhance cardiac
tration has been reported to induce less neurohormo- output, but may lead to other complications; close
nal activation and vasoconstriction. haemodynamic monitoring is essential to direct
therapy.
Intra-aortic Balloon Pump (IABP) Further Reading

IABP use may reduce afterload, thereby decreasing left
ventricular stroke work and myocardial oxygen con- Binanay C, Califf RM, Hasselblad V et al. Evaluation
study of congestive heart failure and pulmonary
sumption, as well as augmenting diastolic blood flow artery catheterization effectiveness: the ESCAPE trial.
in the coronary and systemic circulation. Functional Journal of the American Medical Association. 2005;
mitral regurgitation, a common problem in a patient 294: 1625–1633.
with a dilated left ventricle, decreases with the use of Elkayam U, Ng TM, Hatamizadeh P, Janmohamed M,
the IABP. Mehra A. Renal vasodilatory action of dopamine in
16:10:40
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patients with heart failure: magnitude of effect and site Nohria A, Lewis E, Stevenson LW. Medical management of
of action. Circulation. 2008; 117: 200–205. advanced heart failure. Journal of the American Medical
Felker GM, Lee KL, Bull DA, et al. Diuretic strategies Association. 2002; 287: 628–640.
in patients with acute decompensated heart Steimle AE, Stevenson LW, Chelimsky-Fallick C, et al.
failure. New England Journal of Medicine. 2011; Sustained haemodynamic efficacy of therapy
364: 797–805. tailored to reduce filling pressures in survivors
Francis GS, Bartos JA, Adatya S. Inotropes. Journal with advanced heart failure. Circulation. 1997;
of the American College of Cardiology. 2014; 96: 1165–1172.
63: 2069–2078. Stevenson LW. Management of acute decompensation.
Hochman JS, Sleeper LA, Webb JG, et al. Early In: Mann DL (Ed). Heart Failure, Belvoir Publication,
revascularization in acute myocardial infarction 2004, pp. 579–594.
complicated by cardiogenic shock. SHOCK Investigators. Thiele H, Schuler G, Neumann FJ, et al. Intraaortic balloon
Should we emergently revascularize occluded coronaries counterpulsation in acute myocardial infarction
for cardiogenic shock. New England Journal of Medicine. complicated by cardiogenic shock: design and rationale
1999; 341: 625–634. of the Intraaortic Balloon Pump in Cardiogenic Shock
McMurray JJ, Adamopoulos S, Anker SD, et al. ESC II (IABP-SHOCK II) trial. American Heart Journal.
guidelines for the diagnosis and treatment of acute 2012; 163: 938–945.
and chronic heart failure 2012: The Task Force for the Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/
Diagnosis and Treatment of Acute and Chronic Heart AHA guideline for the management of heart
Failure 2012 of the European Society of Cardiology. failure: executive summary: a report of the American
Developed in collaboration with the Heart Failure College of Cardiology Foundation/American Heart
Association (HFA) of the ESC. European Journal of Association Task Force on practice guidelines.
Heart Failure. 2012; 14: 803–869. Circulation. 2013; 128: 1810–1852.
MCQs
1. Clinical presentation of acute heart failure may (d) Digoxin
include the following symptoms and signs: (e) Hydralazine
(a) Raised jugular venous pressure 4. Regarding inotropic drugs used for the treatment of
(b) Third heart sound patients with acute heart failure:
(c) Peripheral oedema (a) Can be used to improve renal perfusion
(d) Altered mental state (b) High doses of catecholamines can be
arrhythmogenic
(c) Levosimendan is better at improving the symptoms
2. Investigations and monitoring for the patient with of dyspnoea than dobutamine
acute heart failure may include:
(d) All of the above
(a) Pulmonary artery catheter
(e) Enoximone has a short half-life
(b) Systemic vascular resistance
5. Regarding the use of an intra-aortic balloon pump
(c) Mixed venous oxygen saturation which of the following statements is true?
(d) Echocardiography as a first line investigation (a) Both systolic and diastolic blood pressure are
(e) All of the above increased
3. First line drug therapy in the treatment of chronic (b) Haemodynamic effects include an increase in after-
heart failure includes the following: load and increase in cardiac output
(a) Dobutamine (c) Severe mitral regurgitation is a contraindication
(b) Calcium channel blockers (d) Aortic regurgitation is a contraindication
(c) Angiotensin converting enzyme inhibitors (e) Compartment syndrome is an unlikely complication
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Section 7
Chapter
Neurological Aspects of Cardiac Surgery
46 Max S Damian
Introduction patients at risk of developing neurological complica-

tions. In CABG patients generally, the risk of severe
Cardiac surgery’s profound intervention in systemic
carotid stenosis may be higher than in the general
blood pressure and circulation carries a high potential
population, and carotid ultrasound before elective
to affect the brain in a way that may offset the ben-
CABG benefits carefully selected patients the most.
efits of successful cardiac procedures. Astonishing
progress has been achieved in safety and effectiveness,
which has enabled cardiac surgery to become feasi-
ble in ever older and sicker patients. However, these
Neurological Aspects of
are at higher risk of stroke, which in turn increases Cardiopulmonary Bypass and
mortality fivefold, and neurological complications Extracorporeal Oxygenation
prolong intensive care treatment and rehabilitation. Cardiopulmonary bypass has been a prerequisite for
Conditions treated by emergency cardiac surgery, modern cardiac surgery, and in the past 60 years this
such as aortic dissection and acute cardiac failure, has become a safe, routine procedure. Venous blood
carry a high risk of neurological complications even from the systemic circulation is drained to a reser-
without surgery, which may only come to light in the voir, then pumped through a filter and membrane
postoperative period. oxygenator system to the ascending aorta, which is
Cardiac surgeons closely monitor effectiveness cannulated distal to the aortic cross-clamp. In a sec-
and adverse effects, so the complications of cardiac ond venous-to-arterial circuit originating from the
surgery have been well identified. Prevention of neu- bypass, some of the blood is diverted back to the heart
rological complications includes thorough preopera- together with cardioplegia solution, and from the
tive screening and perioperative monitoring, and this heart to the venous reservoir after being purified from
has deepened our understanding of potential risks. embolic material in a cardiotomy reservoir.
This chapter will provide an overview of the most sig- Neurological complications related to the cardiac
nificant neurological problems encountered around bypass are fortunately rare. One main source of prob-
cardiac surgery, their diagnosis and management, and lems is related to embolism, when during preparation
an outline of preventive options. of the cardiopulmonary bypass circuits, cross-clamp-
ing, and turbulent or high-velocity blood flow can
dislodge atheromatous material from the aortic wall.
Neurological Considerations in In addition, bypass circulation requires heparinisa-
Patients Undergoing Cardiac Surgery tion and, together with cardioplegia solution and
Changing patient characteristics indicate a growing other admixtures causing haemodilution, alters the
potential for neurological complications: the age of flow and oxygenation qualities of the blood perfusing
patients in cardiac surgery has increased, and the case the brain. Furthermore, contact between the blood
mix accepted for CABG has also changed through the and non-biological filter membranes and bypass sur-
advent of PCI as an alternative procedure. Competent faces induces a systemic inflammatory response with
preoperative neurological assessment including a potential neurological significance which is not yet
detailed cerebrovascular history may help identify well understood.
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Chapter 46: Neurological Aspects of Cardiac Surgery
A number of technical modifications may help to be lower. It is unclear which systemic blood pres-
reduce the risk of neurological complications. sure is optimal for brain protection during surgery.
Preoperative transoesophageal or intraoperative epi- Trials comparing a mean arterial blood pressure of
aortic ultrasound may help identify patients particu- 50 mmHg with 70 mmHg failed to demonstrate a
larly at risk for embolism related to aortic cross-clamp significant benefit for either approach. Either tar-
and potentially may allow modification of the surgi- get would mean a cerebral perfusion pressure (CPP)
cal strategy. Most procedures with cardiopulmonary lower than the CPP of 70 mmHg currently advised
bypass are performed using mild hypothermia. The for brain protection in acute traumatic brain injury;
importance of temperature management for brain whether this has clinical significance has so far not
protection in hypoxic conditions has been long recog- been investigated.
nised, both for cardiac surgery and for treatment after
cardiac arrest. However, a Cochrane review of studies
comparing neurological outcomes after hypothermic
Acute Neurological Complications of
and after normothermic bypass surgery did not estab- Cardiac Surgery
lish a clear benefit.
Deep hypothermia is used to prolong toleration of Central Nervous System
hypoxia to the brain in surgery with prolonged cere- Stroke is the commonest neurological complication
bral circulatory arrest, for instance aortic arch surgery after cardiac surgery, occurring through embolism
or pulmonary thromboendarterectomy. Although the or hypoperfusion. The incidence of clinically relevant
neuroprotective effect of deep hypothermia is beyond stroke has decreased to under 2% after CABG and
doubt, the precise temperature required to achieve under 4% after single valve replacement, despite the
maximum benefit, the parameters to which hypo- demographic increase in the proportion of elderly at-
thermia should be implemented and how rewarming risk patients. Postoperative diffusion-weighted MRI
should take place remain unclear. Rapid rewarming scans demonstrate clinically silent new lesions in up to
after therapeutic hypothermia can trigger epileptic 18%. Valve replacement and combined CABG and val-
seizures. Other potentially neuroprotective strate- vular surgery procedures carry a higher risk of causing
gies include the use of anterograde or even retrograde embolic territorial and branch infarcts, whereas pro-
selective brain perfusion. The neurological benefits longed cardiopulmonary bypass increases the risk of
have not been established, although some evidence watershed infarcts related to hypoperfusion. In most
suggests that selective anterograde perfusion may cases currently, there is no acute active treatment as
permit procedures to take place in moderate rather major surgery is a contraindication for thromboly-
than deep hypothermia. The use of Alpha-stat meta- sis, but the increasing availability of emergency clot
bolic management or pH stat management, in which retrieval may change the situation. Stroke associated
CPB gas sweep rate is adjusted at lower temperatures with left ventricular assist devices has recently been
to compensate for the hypothermic alkaline drift, shown to benefit from endovascular treatment, if
remains controversial. Proponents of pH stat man- recognised early. One likely consequence will be that
agement believe that it improves oxygen delivery, rapid diagnosis in patients evidencing a neurological
increases cerebral blood flow and thus allows more focal deficit on awakening becomes necessary more
effective cooling of the brain. Alpha-stat management often in the near future, increasing the need for imag-
allowing an alkaline pH during hypothermia, on the ing. Ischaemic and haemorrhagic stroke cannot be
other hand, may improve enzyme activity and protein differentiated clinically, so the different management
function, preserve cerebral autoregulation, and pro- mandates CT scanning of the brain, if emergency MRI
duce less risk of embolism through reduced cerebral is not feasible. Specific locations of ischaemic stroke
blood flow. Which method is more beneficial may are associated with particular risks, such as ‘malignant’
depend on multiple factors, including the age of the complete MCA territory stroke with the risk of life-
patient, but the topic remains controversial. threatening hemispheric swelling, or cerebellar stroke
It still remains to be proven whether ‘off-pump’ with the risk of hydrocephalus and brain stem com-
procedures are significantly safer than conventional pression; both these forms of stroke have high fatal-
cardiac bypass. The risk of postoperative delirium, ity if diagnosed late, but often have good outcomes if
which may prolong intensive care, is also claimed treated with prompt surgical decompression.
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Intracranial haemorrhage is infrequent in cardiac intraparenchymal, subdural, epidural and subarach-

surgery, and is related to a combination of intentional noid, and is often atypical. Intracranial haemorrhage
treatment and effects of bypass on platelet func- warrants neurosurgical consultation and some cases
tion and clotting factors, especially in patients with may need decompression.
previously unrecognised predisposing conditions Encephalopathy is an umbrella term for diffuse
(Figure 46.1). The location of haemorrhage can be brain dysfunction that can be due to multiple different
(a) (b) (c)
(d) (e)
(f) (g)
Figure 46.1 A 39 year old female admitted for redo pulmonary endarterectomy. Postoperatively she was heparinised, but also had low
platelets (66 × 109). Failure to awaken, and right sided weakness prompted imaging. CT showed subdural haemorrhage and bleeding
into two pre-existing, unrecognised arachnoid cysts. (a)–(e) Initial CT scans; (d) tonsillar herniation into the foramen magnum; (e) upward
transtentorial herniation; (f ), (g) CT post hemicraniectomy and cyst decompression shows improvement of midline shift.
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aetiologies. In the acute phase after surgery, encepha- immediate postoperative phase where it can occur as
lopathy manifests as failure to awaken, and global a form of ‘reperfusion syndrome’, for example after
hypoxia or ischaemia of the brain needs to be differ- repair of aortic stenosis, after carotid endarterectomy
entiated from sedative overhang. Elderly patients or or after transplantation when there is a rapid shift of
those with cerebrovascular disease are at greater risk arterial pressures. More often, in patients who have
of encephalopathy. Patients scheduled for CABG are undergone transplantation, PRES is related to toxic-
a population with risk factors for cerebrovascular dis- ity of calcineurin inhibitors, in particular tacrolimus,
ease, with a high prevalence of silent infarcts on preop- where a pronounced tremor is often a feature, or to
erative MRI of the brain. A clinical diagnosis of global many other drugs (Figure 46.2).
encephalopathy demands the absence of a focal neuro- Optic neuropathies are uncommon but well-
logical deficit, which makes a careful examination of recognised complications of cardiac surgery.
oculomotor and other cranial nerve functions impor- Infarction of the optic nerve results in permanent
tant. Dysconjugate eye movements imply the presence monocular loss of visual acuity and visual field defects,
of a focal brain stem lesion, for instance stroke in the with optic disc swelling (anterior optic neuropathy) or
basilar distribution, which may go undetected in rou- without (posterior optic neuropathy). A monocular
tine CT of the brain. Multiple simultaneous emboli can disturbance of vision needs to be differentiated from
simulate global brain dysfunction, making imaging of incongruous hemianopia due to infarction affecting
the brain mandatory as well as extensive metabolic the optic tracts, which does not affect the pupillary
and infectious screening in prolonged encephalopathy. reaction and where the visual field defect in each eye
Negative CT but persistent failure to awaken will mean differs in size. Infarction of the visual cortex causes
an indication for MRI of the brain and/or electrophysi- homonymous hemianopia with an identical visual
ological studies. Lumbar puncture may be needed after field defect in both eyes.
imaging, in the early postoperative period, to exclude
subarachnoid haemorrhage, and in the later postop-
erative period to exclude infection. Peripheral Nervous System
Encephalopathic patients, when they awaken, Brachial plexus injury causes denervation in the distri-
may have persistent confusion or delirium, a fluctu- bution of multiple peripheral nerves, and after median
ating conscious state, or recurrent agitation and hal- sternotomy with sternal retraction a lower brachial
lucinations. Repetitive movements such as tremor, plexus injury of varying severity occurs in up to 5%
asterixis, choreoathetosis or myoclonus are frequent, of patients. The majority are mild and transient, with
and are often suspected to be epileptic seizures. The sensory and motor symptoms resembling ulnar nerve
clinical diagnosis or exclusion of epileptic seizures injury, although findings on careful examination may
versus movement disorders, stereotypies or parox- show a Horner’s syndrome, or sensory deficits and
ysmal dysautonomia is notoriously unreliable. EEG reflex abnormalities exceeding the distribution of a
is mostly needed to confirm the suspicion and make single peripheral nerve. Persistent and severe defi-
the indication for anticonvulsant drugs. Even in the cits warrant neurophysiological examination, which
absence of abnormal movements or stereotypes, a may help prognostication by estimating the degree
prolonged EEG may be necessary to exclude non- of axonal injury versus demyelination. Intraoperative
convulsive status epilepticus (NCSE). This condition monitoring of sensory nerve conduction may help
has only recently been recognised and its incidence to avoid brachial plexus injury, and identify factors
in cardiosurgical patients is unclear, but it has been which make brachial plexus injury less likely, such as
shown to be prevalent in neurotrauma and in sepsis minimising the opening of the sternal retractor, cau-
patients. A fluctuating dyscognitive state may be the dal positioning of the retractor and reducing asym-
only clinical sign of NCSE, and the features may be metric traction. Transient injury to sympathetic fibres
so unspecific that only EEG may differentiate it from through ipsilateral jugular venous cannulation caus-
other causes of delirium. ing Horner’s sign, but with no abnormalities in the
Posterior reversible encephalopathy is a syndrome arm, is a differential diagnosis to partial lower bra-
of vasogenic oedema affecting predominantly white chial plexopathy.
matter, more often the posterior region of the brain, The phrenic nerve passes through the mediasti-
and is diagnosed by MRI. It is occasionally seen in the num adjacent to the pericardium and is therefore
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Figure 46.2 A 29 year old patient post double lung transplant. Agitation and visual hallucinations developed shortly after initialising
the full dose of tacrolimus. CT scan was unremarkable. MRI shows PRES with symmetric high posterior white matter signal in FLAIR image
sequence.
vulnerable to injury during surgery. The frequency transection. Rare bilateral phrenic nerve palsy causes
of unilateral diaphragmatic weakness due to phrenic failure to wean from the ventilator.
nerve injury may reach 10% after cardiac surgery. Unilateral recurrent laryngeal nerve injury causes
Diaphragmatic weakness causes weakness of inspira- dysphonia; the left side is more often affected due to
tion and atelectasis, and predisposes to postoperative its longer intrathoracic course. Bilateral laryngeal
respiratory complications, especially in the pres- palsy leads to severe stridor and aspiration. Several
ence of pre-existing pulmonary disease. Most cases mechanisms can be suspected, from central venous
recover within months, but weakness may persist if catheterisation to traction along the nerve’s intratho-
there is significant axonal degeneration, as with nerve racic course, for instance traction on the oesophagus,
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385
subclavian arteries, or on the heart. Other mono‑ decline reduced from 29% to 21%, but the difference
neuropathies have been described related to nerve becomes insignificant after 12 months (30.8% versus
compression or trauma during prolonged surgery, 33.6%) and currently no surgical technique has been
including ulnar, radial, long thoracic, spinal accessory, shown to be protective.
peroneal, lateral femoral cutaneous, and facial nerves. Delayed cognitive decline occurring over the
Most of these are related to typical nerve compression 5 years after CABG surgery has been described by
sites, and are seldom persistent. various authors. However, comparative studies have
Intensive care unit acquired weakness (ICU-AW) demonstrated a similar change in patients treated with
is a complication which was originally named critical angioplasty and no difference between neuropsycho-
illness polyneuropathy, but is now recognised to affect logical performance in patients treated with bypass
primarily muscle at least as often, causing an acute CABG and with off-pump CABG. Therefore, the the-
or subacute myopathy. The exact causation remains ory that the delayed decline is causally linked to CABG
unclear, but ICU-AW is most often associated with surgery remains unproven, although it seems that
prolonged ventilation, sepsis and use of steroids and cognitive decline may be linked to an accumulation of
muscle relaxants. Muscle biopsy findings are variable, vascular risk factors, and to the patients’ preoperative
with some cases showing only Type 2 fibre atrophy, conditions. The best preventative measure is therefore
which is an unspecific abnormality, others showing meticulous attention to the control of vascular risk
necrotising myopathy or acute myosin loss. The clue factors postoperatively, and no decline has been dem-
to diagnosis is a patient who after prolonged venti- onstrated where this was the case. Microembolic brain
lation is tetraplegic, fails to wean, but has relatively injuries have been implicated in the genesis of delayed
preserved eye and often facial movements. Nerve con- Alzheimer dementia after cardiac surgery, but there is
duction studies are often normal, electromyography currently no evidence that patients who undergo car-
may be myopathic but is often unspecific, and mus- diac surgery are really at increased risk for dementia
cle biopsy may be needed for confirmation. Crucially, or Alzheimer’s disease, and the significance of micro-
CNS pathology, including spinal cord damage, has to emboli is not yet established.
be conclusively excluded.
Guillain–Barré syndrome (GBS), an autoimmune Complications Specific to Cardiac and Heart
acquired demyelinating neuropathy, may rarely occur
after cardiac or other surgery. In the chronic postoper- and Lung Transplantation
ative phase GBS has been described as a consequence The survival rate today of modern cardiac transplan-
of CMV reactivation after cardiac transplantation or tation is impressive, exceeding 80% at 1 year, 70% at
as a symptom of graft-versus-host disease. Neuropathy 5 years and 50% at 10 years. Neurological complica-
after transplantation can be caused by tacrolimus tox- tions constitute a significant proportion of mortality
icity, or by other commonly used neurotoxic medica- and postoperative morbidity; whether modifications
tions such as amiodarone. of the transplantation procedure such as preoperative
use of ventricular assist devices, or of combining heart
and lung transplantation, have an impact on morbidity
Delayed Neurological Complications is still under investigation. Interestingly, an increasing
number of patients undergo cardiac transplantation
Cognitive Decline after Cardiac Surgery with a known genetic neuromuscular disease caus-
Immediate postoperative neuropsychological impairing cardiomyopathy, but also limb muscle weakness,
ment in the absence of a structural defect is common and the outcomes for these patients are apparently no
but reversible over the course of the days following sur- worse than for patients without underlying neurologi-
gery. A more persistent cognitive impairment, how- cal disease.
ever, wears off over weeks or months; it is considered Patients accepted for cardiac transplantation are
comparable to cognitive problems after non-cardiac likely to have heart failure and a high risk of embo-
surgery, possibly due to brain injury at a cellular level. lism prior to surgery, and some may have needed pro-
Better cognitive performance is seen at 3 months after longed preoperative treatment with ventricular assist
CABG surgery performed off pump compared with devices or ECMO, which themselves carry a substan-
patients undergoing bypass, with a risk of cognitive tial risk of cerebral embolism (Figure 46.3). Until
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(a) (b)
(c) (d)
Figure 46.3 A 26 year old female after fulminant heart failure due to sarcoid cardiomyopathy, with emergency transfer under CPR for
ECMO and ventricular assist device. Imaging took place after encephalopathy and agitation were noted. Initial CT shows a left basal ganglia
infarct (a) and a right occipital cortical infarct (b). MRI shows both watershed infarcts (c) and a left occipital pole infarct (d). There was good
functional recovery after cardiac transplant.
recently, the only treatment option for acute stroke The early neurological complications related to
was thrombolysis, unfeasible for patients who had transplantation surgery itself are similar to those
just undergone heart surgery, but the situation may found after other cardiac surgery, but they are more
change with increasing availability of clot retrieval. frequent. In one series, the frequency of perioperative
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CNS complications in heart transplantation was (PCNS-PTLD) is an uncommon Epstein–Barr virus

19.8% versus 3.1% in routine and 10.3% in emer- driven malignancy that may cause systemic uncon-
gency CABG surgery. The incidence varies widely trolled B-cell proliferation affecting many organs,
between series. Perioperative neurological compli- or primarily affecting the brain and central nervous
cations occurred in 23% in the Mayo Clinic series, system, according to a recent series, in 0.18% of heart
and in other series early complications were even and/or lung transplant recipients. It may regress with
more frequent. Perioperative stroke occurs in up reduction of immunosuppressive treatment, or may
to 11%. Delirium and encephalopathy may occur require radiotherapy or chemotherapy.
in 10–20% of cases, including posterior reversible Pharmacological side effects of immunosup-
leucoencephalopathy. pressive drugs are dominated by the effects of cal-
Seizures are reported in 2% to 20% of patients, cineurin inhibitors, and today in the first line by
often as part of a generalised encephalopathy. Once tacrolimus related side effects. These can be both
embolic stroke has been excluded, the presumed direct toxic effects as well as immune reactions trig-
aetiologies are rapid shifts of brain perfusion and gered by tacrolimus. Calcineurin toxicity affects both
drug effects, particularly of calcineurin inhibitors. the CNS with tremor in early stages, and in more
As these patients are on multiple drugs, the possi- severe cases seizures, encephalopathy, cortical blind-
bility of unexpected interactions always needs to ness and psychosis. Patients may have very variable
be considered. Levetiracetam is today the anticon- MRI findings of the brain, and commonly posterior
vulsant of choice, due to its advantages of availabil- reversible encephalopathy syndrome (PRES) and
ity in intravenous preparation, lack of depression vasogenic oedema, but imaging may be completely
of conscious state and lack of enzyme induction normal despite CNS symptoms. Calcineurin inhibitor
or effects on cyclosporine, tacrolimus or warfarin toxicity may also affect the PNS, causing demyelinat-
levels. CSF studies are necessary in most cases, to ing neuropathy or inflammatory myopathy. Toxicity
exclude early onset of a CNS infection, although is not always closely related to the tacrolimus levels,
infections are more common beyond the immediate but generally improves when the dose is reduced.
perioperative phase. Combination with other immunosuppressants (ster-
In this early period complications related to the oids, mycophenolate, sirolimus) may be helpful to
peripheral nervous system are reported in between minimise the dose, but newer immunosuppressants
4% and 11% of cases, and include both the nerve com- can demonstrate similar side effects. OKT3, another
pression and nerve and plexus traction problems out- less frequently used immunosuppressant, has been
lined earlier in this chapter, as well as immunological seen to cause aseptic meningitis.
complications such as Guillain–Barré syndrome or Infections of the CNS after cardiac transplanta-
early drug toxicity. tion occur in 2–3% of patients of recent larger series
Later after transplantation, neurological compli- including some 600 patients, with a broad range of
cations include many conditions not seen in other potential infectious agents; the incidence of any spe-
types of cardiac surgery, broadening the spectrum cific agent is too low to narrow the range of differ-
of possible differential diagnoses, which emphasises ential diagnoses. Aspergillus species, Cryptococcus
the importance of early accurate identification. In neoformans, Listeria monocytogenes, Herpes zoster
the Mayo Clinic series reported by van den Beek and and JC virus occurred more than once. Aspergillus
coworkers, the risk for neurological complications
is a particular diagnostic concern. Other infec-
over a period of 18 years was 81%, including sleep- tious agents that have been described include
ing disorders in 32%, polyneuropathy in 26% and Streptococcus pneumoniae, West Nile Virus, HHV6,
cumulative risk of stroke in 14%. The cause of death Toxoplasma gondii, Nocardia species, Candida spe-
was neurological in 13%. Severe late complications cies, Cryptococcus, Balamuthia mandrillaris, Bipolaris
are dominated by the effects of stroke and of prob- spicifera, Tuberculosis, Acanthamoeba, Scedosporium
lems related to immunosuppression, including direct and syphilis. ‘Acute flaccid paralysis’ due to West Nile
side effects of immunosuppressive drugs, infection, Virus has not been described after cardiac transplan-
transplant rejection, or post- transplantation lym- tation, but clearly, due to increasing prevalence, it
phoproliferative disorder and other malignancies. needs to be included in the differential diagnosis of
Post-transplantation lymphoproliferative disorder neuromuscular weakness.
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Prevention and Risk Assessment in stenosis, because it can reduce the risk of embolism
and stroke. The benefit of simultaneous CABG and
Cardiac Surgery CEA is not established in asymptomatic high grade
The best strategy to prevent neurological complica- stenosis, but the ACC/ AHA guidelines and other
tions in cardiac surgery remains management of risk authors suggest simultaneous endarterectomy and
factors and thorough assessment of the patient’s risk CABG in patients with high grade stenosis on one
profile. The risk of stroke increases with age, reaching side, and severe stenosis or occlusion on the other.
5% in patients over 80, although results have improved
in newer studies. Other characteristics elevating a
patient’s risk profile for stroke and neurological com- How to Deal with the Patient
plications are the presence of hypertension, diabetes Who Fails To Awaken?
mellitus, smoking, a history of cerebrovascular dis- Failure to awaken after cardiac surgery is a worry-
ease, peripheral vascular disease and aortic atheroma, ing neurological scenario encountered in the early
and the type of surgery required. Intraoperative fac- postoperative phase, and may signify anything from
tors associated with increased risk can be duration of transient encephalopathy to a catastrophic focal
the cardiopulmonary bypass and its haemodynamic event. Patients may be systemically severely unwell,
performance. A postoperative risk factor for stroke is and ongoing procedures such as ECMO and pacing
the presence of atrial fibrillation. wires may limit the feasibility of standard neurologi-
The 2011 ACC/AHA guidelines include recom- cal investigations. On the other hand, new treatment
mendations on prevention of neurological compli- options such as clot retrieval increase the potential
cations. A number of potential strategies are aimed benefit of accurate early diagnosis.
at reducing complications related to cardiopulmo- In the comatose patient, diagnostic evaluation
nary bypass. Shann et al. recommend the following includes bedside clinical assessment, specialist review,
evidence-based strategies: appropriate use of neuromonitoring and neurophysi-
1. Reducing emboli through arterial filtration, ological techniques and timely choice of imaging. Any
intraoperative aortic imaging, minimising direct test is only as good as its availability at the right time,
reinfusion of pericardial suction blood, filtration and a multimodal approach builds on good clinical
of suction blood before reinfusion; evaluation.
2. Minimising the prothrombotic response through Clinical assessment is primarily performed by the
reducing blood contact with non-biocompatible intensive care doctors and nursing staff, and their first
surfaces in CPB; responsibility is to recognise there is a potential neu-
3. Ensuring perioperative normoglycaemia and rological problem as early as possible, whether or not
avoidance of hyperglycaemia; they have specialist neurological expertise. Standardised
4. Avoiding low haematocrit and excessive clinical scores are helpful, as long as their limitations are
haemodilution; recognised and interpretation is consistent. The Glasgow
Coma Score (GCS) is the most widespread tool, but it has
5. Managing rewarming rate and limiting arterial
significant limitations such as having inadequate valida-
line temperature to 37 °C during rewarming;
tion in non-trauma patient groups, including largely
6. Optimising metabolic management (pH stat
irrelevant criteria such as the verbal response, and pro-
versus alpha stat management remains a matter of
viding inadequate information on brain stem function
controversy).
or focal deficits. The clinical evaluation must reliably
The ACC/ AHA guidelines for CABG recommend check for focal dysfunction and brain stem abnormali-
perioperative administration of a beta-blocker drug ties, as either is unusual in generalised encephalopathy.
to reduce the risk of atrial fibrillation, as well as perio- The Full Outline of UnResponsiveness (FOUR) score
perative statins and aspirin. Epiaortic ultrasound is provides better neurological information and in the
advised to identify atherosclerosis of the aorta, and author’s experience more validity in serial examination.
to enable measures to be taken that might help avoid Performance in neurological scores informs a more
embolism, such as choice of off-pump. Simultaneous comprehensive assessment by the neurocritical care
carotid endarterectomy is recommended with CABG specialist, as early as possible. This should ideally set the
for symptomatic high grade (70–99%) internal carotid priorities for imaging and electrophysiological tests.
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Neurophysiological investigations extend the

clinical assessment; they are tailored to the clinical
Conclusion
Cardiosurgical neurology is a unique field in which
situation and are best done after clinical review. EEG
good cooperation between cardiac surgeons, cardiac
is the only method to diagnose non-convulsive sei-
intensivists and intensive care neurologists is signif-
zures. Routine bedside neuromonitoring promises to
icantly improving clinical outcomes. We now have
provide continuous assessment of brain function, but
powerful diagnostic tools applicable to the periop-
is still in its infancy. Continuous electroencephalo
erative situation. There are still major obstacles to
graphy (CEEG) allows real time detection of seizures,
overcome, including improving neurological train-
and may alert to worsening encephalopathy or (less
ing in the CT ICU, improving neurologists’ under-
well) to evolving large focal lesions. It is gaining use
standing of a complex field extending far beyond
in neurocritical care units, but the amount of data
conventional neurology, and in making sophis-
generated is difficult to handle, requiring experienced
ticated neurological investigations available in a
personnel with specialist knowledge and significant
challenging environment within a very tight time
time. EEG trending with specialised analysis software
frame. Currently, the capabilities of technology are
may help overcome the problem but still requires
still limited by personnel and training constraints,
‘raw’ EEG for interpretation. Telemedicine- based
but the clear benefits they offer are rapidly driving
EEG services today enable competent EEG assess-
change.
ment even in remote hospitals. Simplified EEG-based
monitoring systems have not proved their value and
are handicapped by the lack of spatial resolution Learning Points
offered by 2 to 4 channels. Somatosensory evoked • Neurological complications are major
potentials (SSEPs) are used intraoperatively, and in determinants of outcome after cardiac
addition the evolution of serial SSEPs after hypoxia surgery.
gives robust prognostic information. Monitoring of
• Risk assessment prior to surgery takes into
brain perfusion and oxygenation based on transcra-
account age, cerebrovascular risk factors
nial Doppler ultrasound and near infrared spectros-
and comorbidity, type of surgery, and a
copy (NIRS) is under development, but their clinical
detailed neurological assessment to identify
value is not yet clear.
patients at higher risk of neurological
Neuroimaging is indicated if either clinical or
complications.
neuromonitoring data suggest a focal or evolving
• The postoperative neurological assessment must
lesion, as well as in persistent reduced conscious
screen for focal neurological deficits in order
levels. Computerised tomography (CT) is rapid and
to diagnose vascular deficits early, in time to
sensitive in detecting haemorrhage and supraten-
consider revascularisation in the brain.
torial stroke, and feasible in the presence of metal
• Focal neurological deficits in a patient with
implants and electronic devices. Mobile bedside CT
postoperative encephalopathy suggest a
scanners allow imaging in the ICU. CT angiography
structural abnormality rather than drug effects of
is rapid and has largely superceded diagnostic cathe-
generalised hypoxia, and necessitate urgent brain
ter angiography, and CT perfusion studies can detect
imaging.
vasospasm. Magnetic resonance imaging (MRI) has
exquisite sensitivity in the brain stem and cervical • A fluctuating impairment of the level of
spinal cord, which are largely inaccessible to CT, but consciousness may suggest non-convulsive status
it is more cumbersome, slower and is not suitable epilepticus even if abnormal movements or
for unstable patients undergoing ECMO. With the stereotypies are absent.
exception of magnetic material implants, however, • EEG is mandatory to diagnose and adequately
most disadvantages can be overcome through using treat status epilepticus.
modern imaging sequences and some specialised • Lower brachial plexus injuries are the commonest
equipment. MRI is much more sensitive for white mechanical peripheral nerve injuries after sternal
matter lesions, and has much more capability to date retraction in cardiac surgery. Peripheral nerve
lesion onset and provide biochemical and functional injuries need to be clinically differentiated from
imaging than CT. complications related to the central nervous
16:17:58
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system, as neurophysiological tests are often transplant recipients. Medicine (Baltimore). 2010;
unrevealing in the acute phase. 89(3): 166–175.
• Calcineurin inhibitor (tacrolimus, cyclosporin A) Pawliszak W, Kowalewski M, Raffa GM, et al.
toxicity can cause multiple peripheral and central Cerebrovascular events after no-touch off-pump
neurological symptoms. Toxicity does not closely coronary artery bypass grafting, conventional
side-clamp off-pump coronary artery bypass, and
correlate with the individual’s blood levels, but
proximal anastomotic devices: a meta-analysis.
improves with dose reduction. Journal of the American Heart Association. 2016;
• The 2011 AHA/ACC guidelines recommend 5: e002802.
strategies to reduce the risk of neurological Salazar JD, Wityk RJ, Grega MA, et al. Stroke after cardiac
complications. surgery: short-and long-term outcomes. Annals of
Thoracic Surgery. 2001; 72: 1195–1201.
Further Reading Shann KG, Likosky DS, Murkin JM, et al. An evidence-
based review of the practice of cardiopulmonary
Al-Mufti F, Bauerschmidt A, Claassen J, et al.
bypass in adults: a focus on neurologic injury, glycemic
Neuroendovascular interventions for acute ischemic
control, hemodilution, and the inflammatory response.
strokes in patients supported with left ventricular assist
Journal of Thoracic and Cardiovascular Surgery. 2006;
devices: a single-center case series and review of the
132: 283–290.
literature. World Neurosurgery. 2016; 88: 199–204.
van de Beek D, Kremers W, Daly RC, et al. Effect of
Hillis ID, Smith PK, Anderson J, et al. 2011 ACCF/AHA
neurologic complications on outcome after heart
Guideline for coronary artery bypass graft surgery.
transplant. Archives of Neurology. 2008; 65: 226–231.
Circulation. 2011; 124: e652–e735.
van de Beek D, Patel R, Daly RC, et al. Central nervous
Mateen F, van den Beek D, Kremer WK, et al.
system infections in heart transplant recipients.
Neuromuscular diseases after cardiac transplantation.
Archives of Neurology. 2007; 64: 1715–1720.
Journal of Heart and Lung Transplantation. 2009;
28: 226. Wijdicks EF, Bamlet WR, Maramattom BV, Manno EM,
McClelland RL. Validation of a new coma scale: the
Muñoz P, Valerio M, Palomo J, et al. Infectious and
FOUR score. Annals of Neurology. 2005; 58: 585–593.
non-infectious neurologic complications in heart
MCQs
1. The following factors are important for assessing the (d) Duration of cardiopulmonary bypass
risk of neurological complications:
(e) Need for ECMO or VADs
(a) Patient age
3. Which following statement applying to postoperative
(b) Premorbidity epileptic seizures is accurate?
(c) In valvular surgery, which valve is to be replaced (a) EEG is seldom needed to identify the presence
of epileptic seizures even with good clinical
(d) Duration of cardiopulmonary bypass
assessment
(e) Positioning for surgery
(b) A neurologist can reliably exclude epileptic seizures
(f) All of the above on clinical grounds
2. Which of the following is NOT associated with neuro- (c) EEG requires the neurophysiology laboratory and
logical problems and worse 1 year outcome after car- has little value in the ICU
diac transplantation?
(d) A prolonged EEG has much higher value in iden-
(a) Surgery performed in poor clinical status tifying non-convulsive status epilepticus than a
(b) Presence or absence of a pre-existing neuromuscu- routine EEG
lar disorder (e) Phenytoin levels are needed to prove efficacy of
(c) Choice of immunosuppressive agent anticonvulsant treatment
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4. Which of the following statements applies? (c) Dysconjugate eye movements reliably indicate
injury to the brain stem
(a) Early diagnosis of postoperative stroke is important
for prognostic reasons only (d) A normal CT scan rules out significant hypoxic
brain injury
(b) Patients cannot be thrombolised after major sur-
gery, so early treatment is not available
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Section 7
Chapter
Postoperative Delirium
47 Makeida B Koyi, Joseph G Hobelmann and Karin J Neufeld
Introduction Delirious patients are frequently overlooked or

misdiagnosed and prevention strategies are not yet a
Delirium is a psychiatric syndrome produced by an
part of routine care in most surgical units. The grow-
underlying medical aetiology and it is a common com-
ing body of literature demonstrating the negative
plication in the postsurgical setting. It can be difficult
short-term and long- term impacts associated with
to detect and is frequently missed by clinicians. It is
delirium highlights the need to improve recognition,
important to recognise and prevent delirium, given its
treatment and prevention of this syndrome. After
association with serious and costly negative outcomes.
describing the epidemiology, this chapter will review
It is characterised by disturbances of awareness, atten-
prevention strategies, and discuss detection and treat-
tion and cognition including perception, thinking,
ment of postoperative delirium in adult patients.
memory, language and orientation. Psychomotor
behaviour, emotion and sleep–wake cycle are also
observed disturbances in delirium. Often abrupt in Delirium Epidemiology
onset, delirium tends to fluctuate throughout the day
and is variable in severity and duration. It can last Core Features of Delirium
from hours to days, and less commonly for weeks to Delirium presents as a sudden change in ability to
months. think, resulting in faulty attention. Common findings
Negative clinical consequences associated with in delirium include:
postoperative delirium include prolonged hospi- • Inability to attend and concentrate resulting in
talisation, loss of functional independence, reduced disrupted short-term recall and disorientation to
cognitive function, incomplete recovery, delayed time and place;
rehabilitation and death. The duration of delirium
• Change in word finding ability and language
in the intensive care unit setting is correlated with
usage –talk may seem confused and difficult to
an increased cognitive impairment in ICU survivors,
follow;
followed as outpatients up to 1 year after discharge.
• Disrupted visuospatial abilities –clock drawing
Delirium can also be associated with significant dis-
or copying interlocking pentagons;
tress in patients and is frightening for family members
• Changes in emotional tone –uncharacteristic
who stand by and watch the pronounced and often
mood lability and disinhibition;
perplexing changes in the behaviour of a loved one.
In patients who undergo cardiac surgery, delirium is • Change in level of arousal/sleep–wake cycle;
associated with postoperative complications includ- • Perceptual changes including hallucinations
ing respiratory insufficiency and sternum instability. (usually visual);
In the USA, the health care costs due to all episodes • Unusual beliefs, which are often frightening and
of delirium in hospitalised patients range from $38 to not uncommonly include misinterpreting the
$153 billion annually, and among older hospitalised intensions of the medical staff.
medical patients it has been shown to be preventable A recognised feature of delirium is that the symptoms
in up to 40% of cases. can fluctuate in severity throughout the day and night.
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Chapter 47: Postoperative Delirium
Delirium Subtypes • Hip fracture (35–65%);

• Coronary artery bypass grafting (37–52%);
Three subtypes of delirium are distinguished by vary-
ing levels of psychomotor activity: hyperactive, hypo- • Peripheral vascular surgery (30–48%);
active and mixed type. • Infrarenal abdominal aortic aneurysm repair
The hyperactive subtype is associated with: (33–54%).
• Restlessness, psychomotor agitation and The risk of delirium increases with the degree of
seemingly purposeless movement; medical urgency. Emergency surgery is associated
• Aggression on the part of the patient, often with much more delirium (both prior to and after sur-
arising from fearfulness and misinterpretation of gery) compared with elective and outpatient surger-
the intentions of the staff and/or disorientation to ies. The highest risk ratings on the American Society
surroundings; Anesthesiology (ASA) scoring system are associated
with a higher risk of postoperative delirium.
• Easy recognition that something is wrong with
the patient;
• Agitated behaviour that may be misattributed to a Risk Factors
primary psychiatric disturbance; The development of delirium is usually multifactorial
• Alcohol and benzodiazepine withdrawal states involving the interaction of a vulnerable patient with
can be the underlying aetiology; one or more perioperative insults. However, delirium
• Among trauma and surgical patients pure can develop in a young healthy patient if the insult
hyperactivity is rare compared to mixed or is significant enough. Prediction models have been
hypoactive subtypes, making up about 1% of developed in both cardiac and non-cardiac surgery to
delirium presentations. help identify those patients most at risk for postopera-
The hypoactive subtype is associated with the following: tive delirium.
The most important factors include:
• Psychomotor slowing and somnolence –often
misattributed to depression; • Advanced age; and
• Can be difficult to recognise –patients with • Baseline cognitive impairment.
hypoactive delirium do not demand much Other additional factors include:
attention from staff; • Impaired physical function;
• Easy to miss the cognitive changes with • Preoperative depressive symptoms;
superficial interactions –such as asking patients
• Preoperative stroke or transient ischaemic attacks;
only ‘yes/no’ questions;
• Abnormal laboratory values such as low albumin;
• Generally associated with worse outcomes and
• History of alcohol and other substance abuse;
more long-term cognitive effects;
• Invasiveness and length of the surgery.
• Most prevalent subtype (~88%) in surgical and
trauma patients. Other predisposing factors, such as atrial fibrillation
and peripheral vascular disease, and precipitating fac-
The mixed subtype is associated with the following:
tors, such as transfusion of aged red blood cells and
• Alternating states of hypoactivity and agitation; the use of an intra-aortic balloon pump (IAPB), have
• Possibly resulting from the administration of been described in other observational studies. Risk
sedating medications to a hyperactive delirious factors for the development of delirium can be divided
patient; into predisposing and precipitating, and are presented
• About 11% of delirium presentations in surgical in a timeline related to surgical course in Figure 47.1.
and trauma patients.
Aetiological Mechanisms
Incidence and Prevalence Although the pathophysiology is not yet understood,
Delirium is prevalent in all hospital settings and in the neuroinflammation and neurotransmitter dysregu-
postoperative course ranges from 5 to 5 0% depending lation have been implicated as possible mechanisms
on the comorbidity and type of surgery. The incidence involved in delirium. More specifically, impaired
of delirium for the following surgeries is reported as: cerebral oxidative metabolism resulting in increases
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Delirium Risks, Measures and Interventions in Adult Patients Undergoing Surgery
SURGERY
PREOPERATVE PHASE POSTOPERATIVE PHASE
EARLY (Post-Op Day 0 & 1) LATER (Post-Op Day 2 and on)
PREDISPOSING PREOPERATIVE INTRAOPERATIVE PRECIPITATING POSTOPERATIVE

Cognitive impairment PRECIPITATING Early Late
Functional impairment Length and invasiveness of
surgery Low haematocrit Infection
Increased age
RISKS
Cardiogenic shock Decreased PO intake

Severe medical illness with increased ASA score† Extremes in blood pressure
Hypoxaemia or dehydration
Alcohol and/or benzodiazepine dependence and hypoxia
Transfusion of aged red Prolonged Constipation
PRECIPITATING PREOPERATIVE
blood cells intubation or slow Pulmonary embolus
Polypharmacy (5 or more medications)
to recover in PACU
Opioid/benzodiazepine dependence Use of an intra-aortic
Frailty balloon pump (IABP) Pain
BASELINE COGNITIVE SCREENING DELIRIUM SCREENING TOOLS

MEASURES
Mini-Cog CAM-ICU∗ 3D CAM

MOCA ICDSC∗ DOS
MMSE 4AT DSI
Also use delirium screening tool to compare NuDESC And others
postoperatively
PREOPERATIVE INTRAOPERATIVE MANAGEMENT POSTOPERATIVE MANAGEMENT

Minimise sedation
INTERVENTIONS
Review outpatient medication list including Minimise surgical length and

“over the counter medications” invasiveness of procedure Mobilise patient as soon as possible
Minimise benzodiazepine premedication or use Consider decreasing depth of Reduce restraints (includes monitors, lines,
of other deliriogenic medications anaesthesia catheters)
Obtain history from collateral informants about Manage BPs (within zone of Avoid use of benzodiazepines except when
cerebral autoregulation) indicated (e.g. management of withdrawal)
Cognitive status and dementia
History or current substance use Consider use of a regional Adequate pain management including non-opioid
block of pain control Stabilise sleep–wake cycle i.e. patient sitting up
and lights on/shades up during the day,
∗ Tools validated for screening for delirium in mechanically ventilated patients decreased disturbance and low lights at night
† American Society of Anesthesiologist physical status classification system
Figure 47.1 Delirium risks, measures and interventions in adult patients undergoing surgery.
in dopaminergic, noradrenergic, and glutamater- • It documents a baseline to which postoperative

gic activity and decreases in cholinergic activity in performance can be compared, aiding in the
response to stress and inflammation of surgical pro- detection of delirium.
cedures have been hypothesised to contribute to Standardised screening tests are the most efficient way
delirium. to test cognition. Many brief tests are available. Casual
conversation with a patient is not sufficient to assess
for preoperative cognitive deficits. The American
Postoperative Delirium Prevention College of Surgeons’ National Surgical Quality
Strategies Improvement Program suggests using the Mini-Cog
as a cognitive screen of the preoperative geriatric sur-
Preoperative Cognitive and Functional gical patient to establish a cognitive baseline and iden-
Status Screening tify high risk patients. Other tools can also be used
and are listed in Table 47.1. Preoperative functional
Given that pre-existing cognitive impairment is the
status is also an independent risk factor for the devel-
most common independent risk factor across studies,
opment of delirium. Assessing the functional status of
assessing for baseline cognitive impairment is benefi-
a patient by using a screening tool assessing activities
cial for two reasons:
of daily living and frailty can provide risk stratification
• It identifies those patients at highest risk for the for delirium and can also provide information about
development of delirium. the expected course of recovery postoperatively.
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Table 47.1 Screening tools for non-intubated patients
Cognitive screening tools Delirium screening tools

Abbreviated Mental Test (AMT) includes 4AT www.the4at.com
10-item, 6-item and 4-item versions 3D Confusion Assessment Method (CAM)
Clinical Dementia Rating (CDR) Bedside Confusion Scale
Clock drawing test Clinical Assessment of Confusion (CAC)
Days of the week backwards Confusion Assessment Method (CAM), short form
Digit cancellation test Confusion Assessment Method-ICU version (CAM-ICU)*
Digit span –forward and backward Confusion Rating Scale (CRS)
Mini-Cog Delirium Observation Screening (DOS)
Months of the year backward Delirium Symptom Interview (DSI)
Montreal Cognitive Assessment (MOCA) Intensive Care Delirium Screening Checklist (ICDSC)*
Trailmaking Test A Nursing Delirium Screening Scale (Nu-DESC)
Trailmaking Test B Single Question in Delirium (SQiD)
*Tools best used for mechanically ventilated, critically ill patients.

Adapted from AGS 2014.
Preoperative Screening for Comorbid Perioperative Interventions

Disease and Substance Use In addition to baseline patient vulnerability, perio-
perative insults contribute to the development of
Abnormal laboratory values, including glucose,
delirium and several interventions to reduce the risk
sodium, potassium and albumin, which represent
have been described. These include pharmacological
underlying disease or organ system dysfunction, are
as well as procedural interventions. A recent meta-
risk factors for delirium:
analysis indicated that several interventions might
• Hypoalbuminaemia appears to be of particular reduce postoperative delirium.
importance due to its association with fluid • Light sedation versus deep sedation may reduce
management, drug binding and malnutrition; the prevalence of postoperative delirium,
• A blood urea nitrogen (BUN) to creatinine particularly in patients receiving spinal
ratio of greater than or equal to 18 (index of anaesthesia for hip replacements.
dehydration). • Although deeper levels of sedation are
Delirium is associated with preoperative alcohol, ben- associated with increased delirium, use of an
zodiazepine and other substance abuse such as opi- electroencephalographic (EEG) monitor to
oids, and prior stroke or transient ischaemic attack. In measure depth of sedation is not yet routinely
general, collection of historical information from the recommended.
patient or collateral informant is sufficient and routine • Type of general anaesthetic agent does not
cerebral imaging is not required for complete assess- appear to affect the development of delirium
ment of delirium risk. but administering additional ketamine during
Depression has been identified as a risk factor for anaesthesia induction may result in less
postoperative delirium in several studies and has been postoperative delirium.
associated with incomplete recovery to independent • Regional anaesthesia, specifically femoral
functioning after surgery. The pathophysiology of this block and fascia iliaca block, for lower
relationship has not been determined. There are many extremity procedures has been shown to reduce
available tools that can be used to screen for depres- postoperative delirium in the elderly.
sion. Assessment of depression may also help predict • Additional areas of inquiry for delirium reduction
the patient’s motivation for recovery and can help in and improved postoperative outcomes in cardiac
postoperative planning. surgery include personalised management
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of blood pressure within the zone of cerebral should be the goal for the management of the criti-
autoregulation, as predicted through near cally ill patient.
infrared spectroscopy (NIRS) and Doppler Some studies suggest that the prophylactic use
monitoring. of typical and atypical antipsychotics can reduce
postoperative delirium; however the trials have been
small, heterogeneous and of variable quality. At least
Postoperative Interventions one study bears replication in larger trials: a ran-
Medications probably contribute to the complex domised controlled trial of on-pump cardiac surgery
pathophysiology of delirium through opioid and patients with subsyndromal delirium upon imme-
gamma- aminobutyric acid (GABA) receptor ago- diate recovery following surgery, treated with risp-
nism. Moderate quality evidence suggests that opioid eridone versus placebo, demonstrated a significant
medication use is associated with delirium in medical decrease in incident postoperative delirium. While
and surgical patients. It is important to weigh the risks there is more research to be done, the recommen-
of opioid use with the benefits of treating acute severe dations arising from a recent meta-analysis suggest
pain, particularly since uncontrolled pain is also cited that there is no clear evidence for routine prophy-
as a risk factor for delirium. It is best to use the lowest lactic use of antipsychotics for delirium prevention
effective dose for pain control. at this time.
Evidence also suggests that benzodiazepine medi- Several other interventions have not demonstrated
cation use increases delirium in a mixed surgical a reduction in the prevalence or duration of postop-
group of patients. This was demonstrated with higher erative delirium. These include:
doses of benzodiazepines over a 24 hour period and
• Intraoperative controlled hypotension;
with longer acting agents. Studies investigating the
• Neuraxial versus general anaesthesia;
risk of delirium with antihistamine medications such
as diphenhydramine noted a trend toward increased • Long acting morphine postoperatively;
delirium as well. • Postoperative sedation using alpha-2
Adequate postoperative analgesia has been asso- adrenoreceptor;
ciated with decreased delirium incidence. Increased • Use of acetylcholinesterase inhibitors;
levels of pain in the postoperative period have been • Use of anticonvulsants;
independently associated with the development of • Use of histamine (H2) blockers.
delirium. Non- opioid medications should be con-
sidered when possible: gabapentin and non-steroidal General Non-pharmacological
anti-inflammatory drugs are associated in some stud- Interventions
ies with reduced incidence and severity of postopera-
Up to one third of cases of delirium have been shown
tive delirium.
to be preventable among medically hospitalised
Preoperative and postoperative sedation regi-
elderly patients through a bundled approach of non-
mens may have an impact on incidence of delirium.
pharmacological interventions. The bundle consists of
Significantly longer time to recovery in the PACU
the following:
with more cognitive dysfunction following anaesthe-
sia has been demonstrated in 1062 patients less than • Enhancing the patient’s ability to see and hear
70 years of age, receiving a premedication of loraze- with the use of glasses and hearing aids;
pam (2.5 mg) compared to placebo. This suggests that • Encouraging increased mobility including
such premedication is best avoided in older more vul- ambulating at least twice per day;
nerable patients. Dexmedetomidine has been shown • Pain control with non-narcotic agents;
in some studies to be more effective than other seda- • Cognitive stimulation through interaction and
tives (benzodiazepines and propofol) in preventing games and activities;
postoperative delirium, but the results have been • Regular re-orientation through calendars and
mixed. Benzodiazepine use is independently associ- verbal interaction with the patient;
ated with delirium in the cardiac ICU and the Society • Sleep enhancement (i.e. non-pharmacological
for Critical Care Medicine (SCCM) Guidelines sug- sleep protocol and sleep hygiene);
gest that sedation reduction and discontinuation • Nutrition and fluid repletion;
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• Appropriate medication usage; the age of 65 years, history of cognitive impairment

• Adequate oxygenation; or brain injury). See Table 47.1 for a list of delirium
• Prevention of constipation. screening tools that have been used on inpatient units
Medications may be the sole precipitant in up to 39% in non-intubated patients.
of all cases of delirium. The risk of postoperative The Richmond Agitation Sedation Scale (RASS) or
delirium increases significantly with polypharmacy other scales that document arousal may prove to be a
(defined as the use of five or more medications at the very good way of screening for delirium. In a study
same time). Anticholinergics, sedatives-hypnotics and using the RASS in 2000 elderly hospitalised patients,
meperidine contribute to postoperative delirium. For any rating other than that described as ‘awake and
example, ranitidine and famotidine, histamine (H2) alert’ was an independent predictor of adverse clinical
antagonists, are commonly used postoperatively for outcomes resulting in longer hospitalisations and dis-
stress ulcer prophylaxis. Due to anticholinergic activ- charge to a skilled nursing facility. The ‘sleepy’ patient
ity these agents may have an increased delirium risk may be the first clue to a sick patient.
compared to proton pump inhibitors (PPI) and con-
sideration should be given to using the latter. Similarly Diagnosis
benzodiazepines and antihistamines should not be
prescribed routinely for sleep in high risk patients; Getting a History
however if benzodiazepines are part of the patient’s The diagnosis of delirium is based upon a complete
longstanding medical regimen prior to surgery, it medical evaluation, consisting of a thorough history
would be best to continue these as an inpatient given and examination. Collateral informants often pro-
the likelihood of physiological dependence. vide the best information regarding the onset, fluc-
tuation and duration of a patient’s symptoms. Family
Screening for Detection of Delirium members are able to describe how a patient’s current
American Geriatrics Society (AGS) and SCCM presentation differs from the presurgical baseline.
guidelines recommend screening all patients for the Information from nurses, rehabilitation therapists
presence of delirium daily in the ICU setting in an and other clinical staff can be helpful given their time
effort to initiate delirium treatment as early as pos- spent interacting with the patient. Patients who are
sible; daily postoperative screening for older patients initially cooperative with the plan and recommenda-
at high risk for developing delirium is advised and tions of the treatment team but who postoperatively
should be conducted by a health care professional present with decreased participation or refusal may be
trained in the assessment of delirium using a vali- exhibiting one of the first signs of delirium. Altered
dated delirium screening instrument. Two validated social behaviour is a common, early presentation and
bedside screening tools with good sensitivity and it is often misconstrued as a symptom of a primary
adapted specificity for critically ill mechanically ven- psychiatric illness. The patient’s mood may be labile,
tilated patients are: or quickly changing, and can be accompanied with
• The Confusion Assessment Method for the ICU symptoms of apathy, anxiety, paranoia, fear, anger,
(CAM-ICU); irritability or even rarely, euphoria. Differentiating
• Intensive Care Delirium Screening Checklist between symptoms of delirium and an exacerbation
(ICDSC). of a primary psychiatric illness can be difficult; how-
ever, delirium is most likely if the symptoms in ques-
Screening for delirium should begin as soon as the
tion are abrupt in onset, fluctuate in severity over a 24
patient is recovered from anaesthesia in the PACU,
hour period and were not present prior to the surgery.
or is stabilised in the intensive care unit. Following
A high index of suspicion is required to detect delir-
general anaesthesia nearly one half of patients, con-
ium as it is easily missed. Other prodromal symptoms
sidered stable for transfer, were found to be delirious
of delirium include:
when assessed by a psychiatrist or research nurse; of
these patients, one half were still delirious on the next • Insomnia;
postoperative day. Once extubated and on the regular • Vivid nightmares or dreams;
inpatient postsurgical services, screening for delirium • Hypersensitivity to sounds or light;
is indicated at least among high risk patients (over • Anxiety;
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• Irritability or restlessness; patient vulnerable to deficiency (i.e. malnutrition and

• Distractibility; recent heavy alcohol use or absorption defects).
• ‘A subjective sense of difficulty in marshalling General physical exam should focus on identifying
one’s thoughts.’ any sources of infection such as respiratory, digestive
and urinary tract, and should include examination of
the oral cavity for dental infections and abscesses and
Examining the Patient pressure sores/ulcers on the skin. Severity and locali-
Testing of cognition is central to examination of the sation of any complaints of pain may also be impor-
patient and comparison of performance to presurgi- tant clues to understanding the cause of delirium.
cal baseline will help make the diagnosis. The cen-
tral cognitive deficit in the syndrome of delirium
includes difficulty in sustaining and shifting atten- Clinical Investigations, Review of Records
tion. Test for attention by asking the patient to try and Consultations
the following: Medical record and medication administration review
• Saying the months of the year in reverse order can point to a cause of delirium. Nursing notes may
(Pass is getting 7 months in a row without reveal changes in a patient’s behaviour over the course
redirection or hints from the examiner); of a few days suggestive of an incipient delirium.
• Saying the days of the week backwards correctly; Noting the timing of a patient’s onset of symptoms in
• Spelling the word ‘world’ or the patient’s name relation to the initiation of a new medication or the
backward; sudden discontinuation of home medications (such
• Counting backwards from 100. as prescribed benzodiazepines) can point to a possi-
In speaking with the delirious patient, one may note: ble aetiology. Any history of substance abuse, or the
• Difficulty maintaining a conversation or following regular use of alcohol or sedative hypnotics, should
commands; be noted.
In addition to reviewing the vital signs, including
• Disorganised thinking –rambling and irrelevant
pulse oximetry as part of the physical examination,
conversation or incoherent speech;
routine investigations should include:
• Fleeting illusions (misinterpreting a stimulus);
• Hallucinations (perception without a stimulus). • Urinalysis and toxicology;
Altered perception is reported by up to 30% of patients • Full blood count;
and can be frightening. As described with the delir- • Metabolic panel including renal profile;
ium subtypes, altered physical function may be dis- • Liver function tests including ammonia.
played with marked agitation, restlessness or vigilance Depending on the findings of the history and exami-
in hyperactive delirium or marked lethargy, decreased nation, additional laboratory tests include thyroid
mobility, reduced movement or reduced appetite in function tests, cortisol, and B12, folate, syphilis serol-
hypoactive delirium. ogy, ANA, HIV, heavy metal screen, urine porphy-
Particular attention should be paid to the neuro- rins and paraneoplastic antibodies such as anti-Hu,
logical examination, observing any abnormal move- anti-Ma and anti-Ta. If CNS aetiology is suspected
ments with the presence of tremor suggesting a or neurological focal exam is demonstrated, CT/
possible aetiology such as alcohol or benzodiazepine MRI of the head and lumbar puncture are indicated.
withdrawal, or serotonin syndrome. Asterixis may An EEG is an important study to consider especially
signal hepatic or renal failure resulting in metabolic if one’s differential includes delirium, non- convul-
derangements, and a focal neurological exam may sive seizures or delirium due to alcohol withdrawal.
suggest the presence of a stroke or TIA. Every effort An EEG of a delirious patient due to systemic illness
should be made to mobilise the patient and examine or metabolic disturbance will generally show diffuse
truncal stability and gait. Thiamine deficiency result- abnormality with slowed background rhythms over
ing in Wernicke’s syndrome rarely presents with the the occiput. This is in contrast to the EEG of a patient
complete triad of ophthalmoplegia, gait instability who is delirious from alcohol withdrawal as that EEG
and delirium, and so repletion of high dose intrave- is either normal or might show fast dysrhythmia or
nous thiamine should be readily implemented in a occasional seizure discharges. The EEG of a patient
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with non-convulsive status epilepticus will be diag- • In patients unable to walk, physical therapy
nostic with evidence of seizure discharges throughout. or occupational therapy should be engaged to
Finally, a consult from an expert in delirium such carry out an active range of motion exercises or
as a psychiatrist, geriatrician or neurologist may help exercises to be done in bed.
determine the cause of the delirium and differentiate • Getting an agitated patient out of bed and
the symptoms of delirium from those of a primary helping them walk around the unit, or to use
psychiatric disorder. Symptoms found in hyperactive, the toilet, can be a successful way to calm them
hypoactive and mixed delirium can mimic symptoms and avoid the use of sedative or antipsychotic
seen in schizophrenia, depression or bipolar disorder. medication.
Providers should be wary of attributing any new onset • Protecting, improving or restoring the patient’s
psychiatric symptoms or new psychiatric diagnosis sleep–wake cycle by keeping the patient upright
to an actively delirious patient in the postoperative in a quiet, well-lit room during the day, and a
setting. dimmed light and low stimulation environment at
night, is best.
• Delirious patients may misinterpret sensory
Treatment stimuli and incorporate them into symptoms of
The most important approach to treatment of delir-
delirium such as fear, anxiety and delusions. It
ium lies in detecting and correcting the underlying
is best to decrease unnecessary stimuli such as
aetiology. The management of the behavioural agita-
the TV, unless the patient specifically requests to
tion that accompanies hyperactive and mixed delir-
watch it.
ium is often difficult. There is insufficient evidence for
• Ensure that the patient has eyeglasses and hearing
the prophylactic use of antipsychotics such as halop-
aids. Examine for and remove earwax to help
eridol in preventing or decreasing delirium severity
improve hearing.
once it occurs. AGS guidelines suggest that benzo-
• Reorient the patient regularly and provide
diazepines should not be used in the management of
accurate and updated wall clocks and calendars.
agitation except if specifically indicated (i.e. substance
withdrawal or serotonin syndrome) and that the low- • Patients benefit from family or care provider
est doses of either a typical or atypical antipsychotic visits and having family members in the room
should be used only if the patient is at significant at night can provide significant reassurance
risk of harming themselves or others or is distressed to a distressed, disoriented person. A bedside
by hallucinations and delusions. One of the harms of sitter may be needed when no family is present,
antipsychotic prescribing in the course of a delirium is especially for delirious patients with agitation, as
that patients are given these medications indefinitely. this patient will need frequent redirection.
Long-term use of antipsychotics can result in CNS
effects such as extrapyramidal symptoms and tardive Learning Points
dyskinaesia, cardiac abnormalities such as prolonga- • Delirium is a clinical syndrome with disturbances
tion of the QTc interval with increased risk of Torsade in awareness, attention, cognition, psychomotor
de Pointes, and stroke and premature death especially behaviour, emotion and sleep–wake cycle with
in the cognitively impaired geriatric population. These the hypoactive subtype most common in the
agents should be used sparingly and on an as needed postoperative surgical population.
basis and discontinued at the earliest opportunity. • Delirium is a common postoperative
Multicomponent non-pharmacological interven- complication that is associated with significantly
tions have proven highly effective in decreasing the poor short-term and long-term outcomes
occurrence of delirium and should be employed in including increased morbidity and mortality.
delirious patients as well. • Patients with increased age and with pre-existing
• Early mobilisation of the patient with the cognitive impairment are at highest risk of
supervision of medical staff or family is one of developing postoperative delirium.
the most helpful non-pharmacological measures • Prevention of delirium requires the identification
and results in a shorter duration of delirium and of patients at increased risk by routinely screening
better functional outcomes at hospital discharge. for cognitive impairment prior to surgery and
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implementing non-pharmacological strategies in Gusmao-Flores D, Martins JC, Amorin D, Quarantini

the care of surgical patients. LC. Tools for diagnosing delirium in the critically
• High risk patients should be screened for ill: is calibration needed for the less sedated patient?
Intensive Care Medicine. 2014; 40: 137–138.
delirium postoperatively to identify delirium
early in the course and correct modifiable causes. Hshieh TT, Yue J, Oh E, et al. Effectiveness of
multicomponent nonpharmacological delirium
• The prevention, detection and management of interventions: a meta-analysis. Journal of the
delirium are paramount to reduce its impact and American Medical Association Internal Medicine. 2015;
improve postoperative outcomes among the most 175: 512–520.
vulnerable patients. ICU Delirium and Cognitive Impairment Study Group.
ABCDEFs of Prevention and Safety, 2013. Available
Further Reading at: www.icudelirium.org
American Geriatrics Society. Clinical Practice Guideline Inouye SK, Westendorp RG, Saczynski JS. Delirium in
for Postoperative Delirium in Older Adults, 2014. elderly people. Lancet. 2014; 383: 911–922.
Available at: http://geriatricscareonline.org/toc/ Johns Hopkins Medicine. Outcomes After Critical Illness
american-geriatrics-society-clinical-practice- and Surgery (OACIS), 2015. Available at: www.
guideline-for-postoperative-delirium-in-older-adults/ hopkinsmedicine.org/pulmonary/research/outcomes_
CL018. after_critical_illness_surgery/.
Barr J, Fraser GL, Puntillo K, et al. Clinical practice Neto AS, Nassar (Jr) AP, Cardoso SO, et al. Delirium
guidelines for the management of pain, agitation, and screening in critically ill patients: a systematic review
delirium in adult patients in the intensive care unit. and meta-analysis. Critical Care Medicine. 2012;
Critical Care Medicine. 2013; 41: 263–306. 40: 1946–1951.
Fleet J, Ernst T. Clinical Guideline: The Prevention, Pandharipande PP, Girard TD, Jackson JC, et al. Long-term
Recognition and Management of Delirium in Adult In- cognitive impairment after critical illness. New England
Patients. Guys and St. Thomas’ National Health Service Journal of Medicine. 2013; 369: 1306–1316.
(NHS) Foundation Trust, 2011. DTC reference 11055i.
MCQs
1. Which of the following factors has the best evidence 3. Important features of delirium include disturbances
of being associated with an increased incidence of in:
delirium? (a) Ability to focus attention
(a) Epilepsy (b) Sleep–wake cycle
(b) Premorbid cognitive impairment (c) Psychomotor behaviour
(c) Hypertension (d) All of the above
(d) Incontinence (e) None of the above
(e) Pre-existing psychiatric illness 4. Which of the following is the best delirium
2. Which of the following outcomes has been associated screening tool to use in mechanically ventilated
with delirium? patients?
(a) Cognitive impairment at 1 year of follow-up among (a) MOCA
ICU survivors (b) MMSE
(b) Increased institutionalisation following discharge (c) CAM-ICU
from hospital
(d) 4AT
(c) Increased healthcare costs
(e) CAC
(d) Increased risk of death
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5. Which one of the following interventions is rec- (c) Use of a non-pharmacological bundle of interven-
ommended by the American Geriatrics Society tions postoperatively
Guidelines to prevent postoperative delirium? (d) Maintaining the patient on bedrest immediately
(a) Preoperative administration of intravenous after surgery to reduce fall risk
haloperidol (e) Intraoperative EEG monitoring of depth of
(b) Pre-medication prior to surgery with 2.5 mg of sedation
lorazepam
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Section 7
Chapter
Haematological Disorders and
48 Cardiothoracic Intensive Care
Jerrold H Levy, Kamrouz Ghadimi and Ian Welsby
Introduction haemostatic factors administered for managing car-

diac surgical patients with haemophilia undergoing
Cardiac surgical patients are at great risk for bleeding
surgery are recombinant or plasma- derived factor
due to multiple factors. Many of these patients have
VIII for haemophilia A or factor IX for haemophilia
underlying disease states that potentially may add to
B, von Willebrand factor (vWF) concentrates for
the risk for impaired haemostasis. Pharmacological
patients with von Willebrand’s disease, and different
therapy for cardiovascular disease, specifically anti-
therapies for patients with platelet defects including
coagulants and antiplatelet agents, can significantly
platelet transfusions.
contribute to these acquired causes of impaired
haemostasis and bleeding. The additional effects of
high-dose heparin anticoagulation for extracorporeal Haemophilia
circulation, fibrinolysis, platelet activation associated Haemophilia is an inherited X-linked recessive dis-
with cardiopulmonary bypass, hypothermia and dilu- order, with an incidence of ~1 in 5000 male births
tional changes are some of the multiple factors that for haemophilia A (factor VIII deficiency) and 1 in
contribute to an acquired coagulopathy. Although 25,000 male births for haemophilia B (factor IX defi-
pre-existing haematological diseases can further con- ciency). Haemophilia patients develop bleeding into
tribute to bleeding in cardiac surgical patients, most their joints, probably due to the extensive presence
of the acquired haemostatic disorders are relatively of glycosaminoglycans in the synovial surfaces and
uncommon. One of the critical haematological issues the lack of tissue factor. Both forms of haemophilia
that significantly influences perioperative manage- are characterised by low levels of factors VIII or IX.
ment in cardiac surgical patients includes heparin- Patients with haemophilia routinely require ortho-
induced thrombocytopenia (HIT). Other major issues paedic surgery because of repeated bleeding into their
related to hypercoagulability are also a potential issue joints. They may also undergo cardiac surgery. There
that will be covered in understanding HIT and have are specific guidelines developed in the haemophilia
been reviewed elsewhere. literature, and haematological management should
include consultations with a consultant haematologist
Congenital Bleeding Disorders for specific timing and maintenance of factor replace-
ment therapy. Depending on the factor levels, factor
Acquired haemostatic disorders due to pharma-
concentrate replacements should be administered
cological therapy are more common in cardiac
within 10–20 minutes of starting a procedure and lev-
surgical patients. A small percentage of patients
els followed perioperatively to further determine spe-
(approximately 1%) may present with one or more
cific factor replacement requirements for maintaining
of the common congenital bleeding disorders, most
levels in the first few perioperative days.
often haemophilia, von Willebrand’s disease (vWD)
and/or inherited qualitative platelet defects. Although
other disorders may exist in patients, focus will be Von Willebrand’s Disease
on these common congenital haemostatic defects. A critical haemostatic protein is vWF, which is present
Critical to patient management is the evolution of in the circulation as a multimeric macromolecule. Its
purified and recombinant replacement factors. The haemostatic function facilitates platelet adhesion to
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Chapter 48: Haematological Disorders
damaged blood vessels, and has critical importance patients present with a markedly prolonged partial
facilitating platelet aggregation. The macromolecule thromboplastin time and activated clotting time, and
functions as a carrier protein to factor VIII, and cir- can complicate managing anticoagulation with hepa-
culates complex to this coagulation factor. The actual rin for CPB. In patients with factor XII deficiency,
von Willebrand’s disease occurs in an estimated 1% fixed dose heparin should be administered based on
of patients. The most common form of the disease time and/or duration of CPB and/or heparin moni-
is type 1, where vWF levels are 10% to 40%. Type 2 toring using heparin-protamine titrations if available.
is a more complex qualitative vWF defect where the
molecule has a decreased ability to bind factor VIII Inherited Platelet Disorders
(type 2N), or increased (type 2B) or decreased (types Beyond the common problem of acquired platelet
2A and 2M) ability to facilitate platelet-dependent dysfunction due to the use of P2Y12 receptor antag-
vWF functions. Type 3 is the most severe form of the onists (e.g. clopidogrel, prasugrel and ticagrelor),
disease where vWF levels are <10% and factor VIII rare forms of congenital platelet dysfunction include
levels are also low. In addition, patients with severe Glanzmann’s thrombasthenia and Bernard Soulier
aortic stenosis and ventricular assist devices develop disease. Fortunately, most patients with this dis-
an acquired form of the disease due to mechanical ease have a long history of easy bruisability, bleed-
injury and disruption of the larger multimeric form. ing and/or family history. There are reports of these
In patients with type 1 disease, desmopressin ~0.3 μg/ patients undergoing cardiac surgery. In patients with
kg is usually administered intravenously. However, in Glanzmann’s thrombasthenia, there is a defect on the
type 2 and type 3 vWD patients, vWF concentrates are platelet surface for the fibrinogen receptor GPIIb/IIIa
the therapy of choice but should be administered after that prevents platelet aggregation, which is a critical
separation from cardiopulmonary bypass (CPB). component of clot formation. Fortunately, patients
Although few clinical data are available, Bhave may have a long history of bruising, mucosal bleed-
et al. reported one of the larger series of 17 patients ing and other soft-tissue bleeding which should make
undergoing cardiac surgery with CPB that included 13 the clinician suspicious of such a disorder. Of note is
patients with haemophilia A, one symptomatic hae- that recombinant factor VIIa is approved for treat-
mophilia A carrier, one with haemophilia B and two ing bleeding in this patient population. Another rare
with vWD. The cardiac surgical procedures included aforementioned syndrome is Bernard Soulier disease,
ten coronary revascularisations, two aortic valve where patients have thrombocytopenia and a reduced
replacements, two mitral valve repairs, two aortic root ability of the platelets to adhere to the damaged blood
replacements, and one combined aortic valve replace- vessel owing to abnormality of the GPIb/V/IX recep-
ment and coronary revascularisation. All procedures tor on the platelets, therefore preventing appropriate
were managed by factor repletion to maintain normal vWF binding, which is another critical step in plate-
levels. Two patients were re-explored for bleeding at let adhesion and activation. Other additional platelet
1 and 20 days postoperatively. abnormalities include storage pool disorders that may
manifest in variable ways and are another rare cause of
Other Less Common Inherited platelet dysfunction. Again, acquired platelet dysfunc-
Bleeding Disorders tion due to the use of antiplatelet agents is a far greater
issue in cardiac surgical patients.
There is a paucity of information beyond case reports
available for managing many of the other less com-
mon coagulation factor deficiencies. However, puri- Procoagulant Disorders
fied factor concentrates are available for most of the
additional rare factor deficiency states. For many of Heparin Resistance
these patients, fresh frozen plasma/plasma and other ‘Adequate anticoagulation’ for CPB is traditionally
factors including factor concentrates may be impor- determined by the activated clotting time (ACT), a
tant during management. Fortunately, many of these whole blood haemostatic activation test that is influ-
patients come previously diagnosed with their spe- enced by multiple causes. Heparin resistance has
cific coagulation deficiency. Factor XII deficiency has been frequently reported in the literature, often due
important implications for cardiac surgery because to a variety of causes. The definition commonly used
16:21:02 403
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404
for heparin resistance is ACT <480 seconds following pathophysiology is due to an antibody that develops
addition of 500 U/kg of heparin. Unfortunately, the following heparin administration to a specific alpha
terminology we use for heparin resistance is a misno- granule protein released from platelets called platelet
mer, because actual resistance does not occur; rather factor 4 (PF4). When PF4 is released, it fuses with the
there is an alteration in heparin dose responsiveness platelet membrane to form a new epitope/antigen,
and an alteration of the slope of the heparin response and as a result immunoglobulin (Ig) G develops that
curve. The ACT actually increases following heparin binds to PF4 complexes on platelets, causing activa-
administration, but not in a linear fashion. tion, sequestration and microparticle formation,
Multiple factors are responsible for producing altered all of which have profound prothrombotic effects.
heparin dose responses, in addition to antithrom- Patients following cardiac surgery and CPB are at an
bin, including preoperative heparin use, high and low increased risk of producing the antibodies which may
platelet counts (both thrombocytosis and thrombo- occur in up to 50% of patients although potentially at
cytopenia), altered platelet function and use of other low levels. The presence and the level of the antibod-
anticoagulants. The association between decreased ies are associated with an increased risk for adverse
preoperative antithrombin and heparin resistance is events, and occur in approximately 1–5% of patients
complicated by multiple factors that affect the ACT who receive unfractionated heparin, although cardiac
in addition to antithrombin levels. Ranucci et al. sug- transplant patients may be at an even higher risk for
gested a 10% predictive chance of a patient developing HIT (~11%).
altered heparin dose responsiveness/heparin resistance.
Antithrombin (also called antithrombin III) is a serine Diagnosis
protease inhibitor that circulates in the plasma at 80– HIT should be suspected if the platelet count drops
110% assuming normal levels, approximately 2.4 µmol. by 50%, or new thrombosis occurs in a patient 5 to
Antithrombin is associated with altered heparin respon- 14 days after the start of heparin therapy. The 4T score
siveness due to the fact that heparin requires the cofac- (thrombocytopenia, timing of platelet count fall,
tor of antithrombin to inhibit factors Xa and thrombin thrombosis or other sequelae, and other causes for
(IIa). Antithrombin is activated by binding to heparin thrombocytopenia) has also been used to determine
via the pentasaccharide sequence of heparin; the rela- the probability of HIT and is thought to correlate well
tive chain length of the sequence controls the binding with antibody formation. However, in cardiac surgical
selectively to factor Xa and/or IIa. Multiple investiga- patients in the perioperative setting, thrombocytope-
tors have noted that previous heparin administration nia is a common problem and is due to multiple causes
decreases antithrombin levels, and produces alterations including dilutional changes post CPB, intra-aortic
in heparin dose responsiveness. balloon pump presence and mechanical destruction,
Multiple reports note that antithrombin improves sepsis or other drug-induced causes, especially IIb/
intraoperative anticoagulation, improves periopera- IIIa inhibitors. Following cardiac surgery and CPB,
tive haemostasis and reduces biochemical markers of HIT may present in a biphasic pattern. Several days
coagulation. Antithrombin administration to correct postoperatively, the platelet count begins to normal-
decreased levels of antithrombin would potentially be ise after CPB-related thrombocytopenia, followed by
of benefit to all patients, as antithrombin levels fall to a decreasing platelet count >4 days postoperatively.
<50% during CPB. Although Linden et al. suggest ther- Following heparin administration intraoperatively, an
apeutic antithrombin is not of added benefit in heparin acute hypersensitivity response may occur due to pre-
resistance because patients do not exhibit decreased existing IgG levels, with hypotension, other systemic
antithrombin concentration compared with heparin responses and acute thrombocytopenia. HIT can also
responsive patients, this is not the case. Antithrombin occur weeks after heparin exposure and is termed
administration will consistently increase ACT respon- ‘delayed-onset HIT’ but this is less common.
siveness in vitro and in vivo as previously reported.
Laboratory Testing
Heparin-Induced Thrombocytopenia Although suspicion of HIT is of critical importance
Heparin-
induced thrombocytopenia (HIT) is a to stop use of heparin and facilitate another antico-
prothrombotic disease where an anticoagulant has agulant, laboratory testing is an important adjunct to
the potential to produce a procoagulant effect. The making the correct diagnosis. The standard testing
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includes antibody determination for screening and For patients requiring cardiac surgery and CPB,
functional assay for definitive diagnosis. Antibody although alternative anticoagulants can be used, hepa-
testing includes a standard enzyme-linked immuno- rin is still the best agent due to its acute reversibility.
sorbent assay (ELISA) that detects either polyclonal For patients with current HIT who require cardiac
antibodies or IgG specific antibodies to complexes surgery, if elective, the surgery should be delayed until
of PF4 and heparin. ELISA results are commonly heparin- PF4 antibodies are negative. Alternatively,
reported to clinicians as either positive or negative; plasmapheresis has been recommended and used
specific information regarding optical density (OD) successfully to manage patients. However, alternative
should also be obtained to facilitate clinical decisions anticoagulation for CPB is best performed with biva-
regarding management and/or further workup. Based lirudin, based on all of the reported data.
on the time of sampling, ‘high-titer negative’ ELISA
results have the potential to become positive several
days later if retested. More importantly, higher optical
Managing HIT Patients for Cardiovascular
density results are associated with increased probabil- Surgery
ity for true HIT, based on published data that will be
discussed later. The serotonin release assay (SRA) and Antibody Positive
platelet aggregation testing are functional assays that If the SRA is negative, then heparin can be used for
are only undertaken in specialised laboratories. CPB but avoiding heparin re-exposure postoperatively
Warkentin et al. reported a study that is important should be considered. If the patient is HIT positive and
for clinical management and is based on antibody SRA is either positive and/or not available and cardiac
testing. In this study, the magnitude of positive ELISA surgery cannot be delayed, either plasmapheresis or
results, as determined by optical density (OD) units, the use of an alternative anticoagulant (specifically
was correlated with functional platelet serotonin- bivalirudin) should be considered, based on ACCP
release assay (SRA) results, the gold standard for guidelines. The most extensive practical clinical and
determining whether a patient is indeed HIT positive. reported experience with an alternative non-heparin
They reported that if the results were weakly positive, anticoagulant is with the direct thrombin inhibitor
0.40–1.00 OD units, the ELISA had a low probabil- bivalirudin. Although dosing guidelines have been
ity of 5% or less for a positive SRA. However, the risk reported for the use of argatroban for CPB, based on
increased to ~90% with an OD of >2.00 units. Their retrospective analysis of 21 adult cases, there is far more
study evaluated 1553 patient sera and reported that extensive experience with bivalirudin. Argatroban for
for every increase of 0.50 OD units in the ELISA-IgG, postoperative anticoagulation in the intensive care
the risk of a positive SRA increased by OR = 6.39, and unit, however, is a potential heparin alternative.
for every increase of 1.00 OD units in the EIA-IgG, the
risk increased by OR = 40.81. Bivalirudin
The most extensive experience with an alternative
Treatment anticoagulant for CPB or off- pump cardiac sur-
Postoperatively, in patients with clinical suspicion of gery is with bivalirudin as previously mentioned.
HIT or confirmed HIT, stopping heparin and starting One of the initial series for coronary artery bypass
an alternative anticoagulant, most commonly the direct grafting using CPB and bivalirudin anticoagulation
thrombin inhibitor bivalirudin or argatroban, are used a 1.5 mg/kg loading dose before cannulation
mainstays of therapy. The alternative danaparoid is not and continuous 2.5 mg/ kg/
hour infusion during
available in most countries. Management for CPB will CPB. Anticoagulation was monitored using a target
be considered separately. As previously mentioned, the ACT of 2- to 2.5-fold over baseline (approximately
4T score has been suggested to determine the relative 300–350 seconds), but with the prolonged half-life
risk of true HIT. Low molecular weight heparin should and lack of reversibility, caution should be consid-
not be used because of potential cross-reactivity with ered targetting normal ACT values. Anticoagulation
antibodies. Anticoagulation with warfarin should be during CPB was effective, and total operating times
avoided based on guidelines until platelet count recov- were acceptable. One patient experienced excessive
ers. Heparin should be avoided, if possible, at least as postoperative bleeding. Prospective studies have
long as heparin-PF4 antibody testing is positive. evaluated bivalirudin (versus heparin) in non-HIT
16:21:02 405
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patients undergoing cardiac surgery using CPB or • Factor repletion is the mainstay of therapy for
undergoing coronary artery bypass grafting without patients with factor deficiency states such as
CPB. Across the studies, bivalirudin was adminis- haemophilia or von Willebrand’s disease.
tered to 206 patients and provided effective anti- • Heparin-induced thrombocytopenia
coagulation with a safety profile similar to that of (HIT) is another important immunological
heparin. Bivalirudin dosing in surgery without CPB haemostatic disorder characterised by
is similar to that used in PCI. prothrombotic potential after heparin
Surgical techniques that allow blood to stay administration.
stagnant should be avoided when using bivalirudin, • Management of HIT patients includes
which is metabolised by enzymes present in blood recognition, monitoring and avoidance of heparin
exposed to wound or foreign surfaces. Therefore, as an anticoagulant.
direct retransfusion of shed pericardial/ medias- • For management of cardiac surgical patients
tinal blood into the cardiotomy container should undergoing cardiopulmonary bypass (CPB)
be avoided during bivalirudin administration in who have been diagnosed with HIT, bivalirudin
order to avoid systemic activation and circulation as an alternative anticoagulant is a mainstay of
of thromboemboli. Alternatively, shed pericardial therapy. Argatroban is another direct thrombin
blood can be processed via cell salvage systems inhibitor which can also be used for postoperative
when using bivalirudin. anticoagulation but there are far less data for its
use during CPB.
Managing HIT Patients in the ICU
Standardised criteria such as the 4Ts clinical scoring
system and platelet profiles can be used to appro-
Further Reading
priately send for PF4/heparin antibody testing and Bhave P, McGiffin D, Shaw J, et al. Guide to performing
cardiac surgery in patients with hereditary bleeding
immediately initiate argatroban. Often clinicians
disorders. Journal of Cardiac Surgery. 2015;
delay initial anticoagulation therapy on clinical sus- 30: 61–69.
picion of HIT due to safety concerns about bleed-
Despotis GJ, Avidan MS, Hogue (Jr) CW. Mechanisms
ing. The lack of increased risk for adverse events and attenuation of hemostatic activation during
with argatroban in the cardiothoracic ICU after sur- extracorporeal circulation. Annals of Thoracic Surgery.
gery suggests early therapy with argatroban as a DTI 2001; 72: S1821–S1831.
should be considered. Other DTIs currently available Dyke CM, Smedira NG, Koster A, et al. A comparison
for use include the parenteral agents lepirudin, desir- of bivalirudin to heparin with protamine reversal
udin and bivalirudin, and the direct oral anticoagu- in patients undergoing cardiac surgery with
lant, dabigatran. The results from our study support cardiopulmonary bypass: the EVOLUTION-ON study.
argatroban use upon immediate clinical suspicion of Journal of Thoracic and Cardiovascular Surgery. 2006;
HIT as detected by an otherwise unexplained drop 131: 533–539.
in platelet count of >50% at approximately 5–10 days Levy JH. Heparin resistance and antithrombin: should it
after surgery. In addition, argatroban use is endorsed still be called heparin resistance?[comment]. Journal
in thrombotic complications for all patients after of Cardiothoracic and Vascular Anesthesia. 2004;
18: 129–130.
cardiothoracic surgery, and prior to confirmation
of laboratory results. Additional prospective, ran- Levy JH, Despotis GJ, Szlam F, Olson P, Meeker D,
Weisinger A. Recombinant human transgenic
domised studies are needed to support our findings,
antithrombin in cardiac surgery: a dose-finding study.
and to determine the relative safety of argatroban and Anesthesiology. 2002; 96: 1095–1102.
other DTIs.
Levy JH, Faraoni D, Spring JL, Douketis JD, Samama CM.
Managing new oral anticoagulants in the perioperative
Learning Points and intensive care unit setting. Anesthesiology. 2013;
• Most congenital bleeding disorders for cardiac 118: 1466–1474.
surgical patients are relatively rare; however these Levy JH, Key NS, Azran MS. Novel oral
patients can also develop cardiac disease and anticoagulants: implications in the perioperative
setting. Anesthesiology. 2010; 113: 726–745.
require cardiac surgery.
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Levy JH, Montes F, Szlam F, Hillyer CD. The in vitro effects Sniecinski RM, Chandler WL. Activation of the hemostatic
of antithrombin III on the activated coagulation time system during cardiopulmonary bypass. Anesthesia &
in patients on heparin therapy. Anesthesia & Analgesia. Analgesia. 2011; 113: 1319–1333.
2000; 90: 1076–1079. Sniecinski RM, Hursting MJ, Paidas MJ, Levy JH. Etiology
Levy JH, Weisinger A, Ziomek CA, Echelard Y. and assessment of hypercoagulability with lessons
Recombinant antithrombin: production and role in from heparin-induced thrombocytopenia. Anesthesia
cardiovascular disorder. Seminars in Thrombosis and & Analgesia. 2010; 112: 46–58.
Hemostasis. 2001; 27: 405–416. Warkentin TE, Sheppard JI, Moore JC, Sigouin CS,
Mannucci PM. Treatment of von Willebrand’s disease. Kelton JG. Quantitative interpretation of optical
New England Journal of Medicine. 2004; 351: density measurements using PF4-dependent enzyme-
683–694. immunoassays. Journal of Thrombosis and Haemostasis.
2008; 6: 1304–1312.
MCQs
True or False (c) Is less common in patients who have been on
1. Common congenital bleeding disorders include: heparin preoperatively
(a) Haemophilia (d) Is associated with high antithrombin levels
(b) Protein C/S deficiency (e) Can be treated by administration of antithrombin
(c) von Willebrand’s disease 4. Heparin-induced thrombocytopenia (HIT):
(d) Bernard Soulier disease (a) Is a prothrombotic disease
(e) Heparin-induced thrombocytopenia (b) Is antibody mediated
2. Von Willebrand’s: (c) Is associated with complexes between PF8 and

heparin
(a) Factor inhibits platelet adhesion to damaged blood
vessels (d) Should be suspected if the platelet count
increases by 50%
(b) Factor is a carrier protein to factor IX
(e) Diagnosis is confirmed by the 4T score
(c) Disease occurs in an estimated 1% of patients
5. Treatment for HIT includes:
(d) Disease can occur as an acquired form
(a) Platelet transfusion
(e) Disease may be due to qualitative or quantitative
defects in VWF (b) Argatroban
3. Heparin resistance: (c) Plasmapheresis
(a) Is defined as ACT < 280 seconds following addition (d) Bivalirudin
of 500 U/kg of heparin (e) Low molecular weight heparin
(b) Is due to an alteration in heparin dose
responsiveness
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Section 7
Chapter
Pregnancy and Cardiovascular Disorders
49 Kiran Salaunkey
Introduction Cardiovascular Physiological Changes

There is an increasing prevalence of cardiovascular in Pregnancy
disease (CVD) in women of child bearing age. It is Though there are widespread metabolic changes in
estimated that about 0.2–4% of all pregnancies in the the pregnant female, for the purposes of this chapter
developed world have cardiovascular complications we will confine our discussion to the cardiovascular
despite no known prior disease. CVD is a major cause changes that occur during pregnancy
of non-obstetric death amongst expectant and new Pregnancy has a profound effect on the circulatory
mothers in the UK. Hypertensive disorders are the system to meet the additional metabolic demands of
most frequent CVD during pregnancy, occurring in the mother and the foetus.
6–8% of all pregnancies. The placenta invades maternal uterine tissue early
The improved longevity following successful medi- in pregnancy and releases an array of hormones and
cal and surgical treatment of congenital heart diseases other factors. These hormones create physiological
has led to an increased number of women becoming changes in the mother, which favour nutrient and oxy-
pregnant with treated congenital heart disease, with gen delivery to the growing foetus.
an increased predominance of shunt lesions. There is an increase in red cell mass and increase
In the developing world the burden of valvular in blood volume, causing increased preload. However,
heart disease among pregnant women persists, but there is dilutional anaemia due to a disproportionate
these issues are also seen in the developing world increase of the plasma component of blood as com-
amongst immigrant populations. pared to its cellular component.
Increased prevalence of risk factors for athero- Further increases in cardiac output by about 20–
sclerotic disease along with an increased maternal age 50% are achieved by an increase in stroke volume of
has led to an increased incidence of coronary artery about 15–30% in early pregnancy and an increase of
disease. heart rate by about 15–30%, mainly towards the latter
Cardiomyopathies, though rare, cause significant stages as caval compression prevents further increases
morbidity. Peripartum cardiomyopathy (PPCM) is in stroke volume.
the most common cause of severe complications. There is a decrease in total vascular resistance by
CVD in pregnancy poses a challenging scenario about 30% due to increased flow into the uteroplacen-
due to changes in the maternal physiology adversely tal circulation, coupled with secretion of vasodilatory
affecting the suboptimal cardiovascular system. The substances from the placenta such as nitric oxide and
responsibility of the treating physician in these cases prostaglandins. The systolic blood pressure for the
ranges from prenatal counselling, antenatal and post- most part remains unchanged but the mean arterial
natal care of the mother and also potentially extends pressure is reduced initially but increases towards the
to the care of the unborn foetus. Considering the dif- end of pregnancy.
ficulties of conducting research in this area, it is not The cardiac performance improves with pro-
surprising that robust prospective randomised studies gressive LV remodelling during pregnancy. There is
are lacking. dilatation of the heart by about 30% with eccentric
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Chapter 49: Pregnancy and Cardiovascular Disorders
hypertrophy. These changes tend to resolve within 2 of pregnancy sometimes manifests as left axis devia-
weeks of postpartum state. tion, increased R wave amplitude in V1 and V2, T
By the second trimester the enlarging uterus will wave inversion in V2, small Q wave in lead II, III and
cause a degree of aortocaval compression, reducing aVF, and inverted T wave in lead III, V1–V3.
the amount of venous return in the supine position. There is an increase in the rate of maternal arrhyth-
A series of haemostatic changes, such as increased mias during pregnancy.
platelet adhesiveness and increased concentration of Further analysis of rhythm disturbances may war-
coagulation factors, leads to a hypercoaguable state; this, rant exercise ECG, tilt table testing and electrophysi-
coupled with stasis due to caval compression described ological studies.
above, can increase the risk of deep vein thrombosis.
Further during labour, pain, anxiety and uterine Echocardiography
contractions cause increased cardiovascular stress.
This is the preferred mode of cardiac imaging due to
Efforts to mitigate pain with neuraxial anaesthesia or
its non-invasive nature, safety profile and reproduci-
intercurrent haemorrhage during delivery affect car-
bility. The transthoracic route is preferred to the trans‑
diovascular performance.
oesophageal (TOE) route.
Post delivery, the phenomenon of autotransfusion,
In cases where TOE is used, care must be taken
resorption of oedema and uterine involution places a
regarding aspects such as gastric stasis, reflux and
significant stress on the cardiovascular system.
sedation needs, which might impact on foetal well
There is a reduction in cardiac output in the post-
being, necessitating foetal monitoring.
partum period.
Diagnosis of Cardiovascular Diseases Exercise Testing

This provides an objective quantification of cardiopul-
History and Clinical Examination monary function especially in patients being followed
A thorough history, specifically looking to elicit famil- up for grown-up congenital heart disease (GUCH)
ial history of cardiomyopathies, Marfan syndrome, and valvular heart disease. It should preferably be per-
long QT syndromes and sudden deaths, should be formed in the prenatal period to help with risk assess-
sought. Assessment of progression of ongoing breath- ment and prenatal counseling.
lessness is a good prognostic tool to predict heart fail- The European Society of Cardiology (ESC) recom-
ure. History should include baseline functional status mends that in asymptomatic patients it is advisable to
and previous cardiac events as these are strong predic- use exercise testing to attain 80% of maximal capacity
tors of peripartum cardiac events. during pregnancy. The safety of exercise testing during
The strongest predictors are: pregnancy has not been established, but there is no evi-
• Any prior cardiac event; dence that it increases the risk of spontaneous abortion.
• Cyanosis or poor functional status;
• Left sided obstruction; Magnetic Resonance Imaging
• Ventricular dysfunction. This is a useful modality that will provide informa-
Examination is directed towards looking for signs tion for diagnosis and therapy. It is probably safe in
of heart failure; if new signs or murmurs are found, the second and third trimesters. It can also be used
this mandates further investigations. Blood pressure to diagnose foetal neurological defects identified by
is measured either at home or in the clinic in the left ultrasound.
lateral recumbent position. Gadolinium ions are known to cross the placen-
Urinalysis for glucose and proteinuria should be tal barrier; the safety of gadolinium is not known in a
performed. developing foetus and should be avoided.
Electrocardiography Cardiac Catheterisation

A standard 12 lead ECG, which is a safe and inexpen- If needed in a pregnant patient, this should prefer-
sive screening tool, should be used. The normal ECG ably be undertaken by the radial route, limiting the
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radiation exposure time and shielding the foetus from dysfunction. The blood pressure readings should be
direct radiation. documented on at least two occasions at least 4 hours
Electrophysiological studies or ablation if needed apart. Gestational hypertension is severe when sys-
should use an electroanatomical mapping system in tolic blood pressure is ≥160 mmHg and/or diastolic
conjunction with MRI to reduce radiation dose. blood pressure is ≥110 mmHg on two consecutive
blood pressure measurements at least 4 hours apart.
Chest X-rays and CT Scans Gestational hypertension is a temporary diag-
nosis for hypertensive pregnant women who do not
A single diagnostic investigation requiring radiation
meet the criteria for pre-eclampsia (see Table 49.2)
exposure is not sufficient to threaten the well being of
or chronic hypertension (hypertension first detected
the developing foetus. However, frequency of expo-
before the twentieth week of pregnancy). The diagno-
sure, and accumulated dose of radiation, do result in
sis is changed to:
adverse foetal effects such as foetal cell death, tera-
togenesis, carcinogenesis and mutations in germ cells • Pre-eclampsia, if proteinuria or new signs of end-
in the foetus. organ dysfunction develop;
A radiation dose below 50 mGy to the pregnant • Chronic (primary or secondary) hypertension, if
mother is the accepted level of radiation below which blood pressure elevation persists ≥12 weeks post
there is no evidence of increased foetal risk. partum;
If ionising radiation is used, its dose should be doc- • Transient hypertension of pregnancy, if blood
umented in the record and the principle of ALARA ‘as pressure returns to normal by 12 weeks post
low as reasonably achievable’ should be used. partum.
The foetus as a rule is protected by the mother’s Thus, reassessment up to 12 weeks post partum is nec-
abdomen and the exposure to radiation is far below essary to establish a final diagnosis.
the level of exposure of the mother. Gestational hypertension occurs in 6– 17% of
Table 49.1 gives the amount of radiation exposure healthy nulliparous women and 2–4% of multiparous
for common radiological procedures. women. Previous history of pre-eclampsia, multifoe-
tal pregnancies and raised body mass index are the
Common Cardiovascular Disorders significant risk factors.
Hypertensive Disorders of Pregnancy Diagnosis

Definitions Blood pressure monitoring is the cornerstone on
Gestational hypertension is a clinical diagnosis which the diagnosis is made; home blood pressure
defined by the new onset of hypertension (systolic monitoring is useful to differentiate white coat hyper-
blood pressure ≥140 mmHg and/or diastolic blood tension. It is important to differentiate gestational
pressure ≥90 mmHg) at ≥20 weeks of gestation in hypertension from pre-eclampsia and pre-eclampsia
the absence of proteinuria or new signs of end-organ from severe pre-eclampsia.
Table 49.1 Estimated foetal and maternal effective doses for various diagnostic and interventional radiology procedures
Procedure Foetal exposure Risk of childhood cancer

Chest radiograph (PA and lateral) 0.001–0.01 mGy <1:100,000
CT chest (including CTPA) 0.01–0.1 mGy <1:100,000
Lung perfusion scan 0.1–1 mGy 1:100,000 to 1:10,000
CT chest abdomen pelvis 10 mGy 1:10,000 to 1:1000
Coronary angiography 1.5 mGy 1:10,000 to 1:1000
PCI or radiofrequency catheter ablation 3 mGy 1:10,000 to 1:1000
CT computed tomography; PCI percutaneous coronary intervention; PA posteroanterior.

Natural childhood cancer risk 1:500.
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Table 49.2 Diagnosis of pre-eclampsia

Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on two occasions at least 4 hours apart after 20 weeks of
gestation in a previously normotensive patient. If systolic blood pressure is ≥160 mmHg or diastolic blood pressure is ≥110 mmHg,
confirmation within minutes is sufficient
AND
Proteinuria ≥0.3 g in a 24-hour urine specimen or protein (mg/dl)/creatinine (mg/dl) ratio ≥0.3
Dipstick ≥1+ if a quantitative measurement is unavailable
In patients with new-onset hypertension without proteinuria, the new onset of any of the following is diagnostic of pre-eclampsia:
Platelet count <100,000/µl Liver transaminases raised to twice normal limits
Serum creatinine > 100 µmol/l OR doubling of serum creatinine in the absence of renal disease
Cerebral or visual symptoms Pulmonary oedema
Table 49.3 Diagnostic features of severe pre-eclampsia

Symptoms of nervous system dysfunction
New onset cerebral or visual disturbance, such as:
• Photopsia, scotomata, cortical blindness, retinal vasospasm
• Severe headache (i.e. incapacitating, ‘the worst headache I’ve ever had’) or headache that persists and progresses despite analgesic
therapy
• Altered mental status
Hepatic abnormality:
Severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by an alternative diagnosis
or serum transaminase concentration ≥ twice normal, or both
Severe blood pressure elevation:
Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg on two occasions at least 4 hours apart while the patient is
on bed-rest (unless the patient is on anti-hypertensive therapy)
Renal abnormality:
Progressive renal insufficiency (serum creatinine >100 µmol/l or doubling of serum creatinine concentration in the absence of other renal
disease)
Thrombocytopenia:
<100,000 platelets/µl Pulmonary oedema
Table 49.3 gives the diagnosis of severe Management

pre-eclampsia. Delivery minimises the risk of development of serious
Foetal well being should be evaluated with esti- maternal and foetal complications due to pre-eclampsia.
mation of foetal weight; umbilical artery Doppler is The management decision is a trade-off between:
helpful for foetuses with intrauterine growth restric-
• The foetal benefits from expectant management
tion. An abnormal Doppler profile is highly specific
(i.e. further growth and maturation);
for severe pre-eclampsia.
• The maternal and foetal benefits from early
HELLP syndrome represents a severe form of
intervention (i.e. avoidance of complications
preeclampsia. It is characterised by:
from progression of hypertensive disease over the
• Haemolysis with a microangiopathic picture on remainder of pregnancy); and
blood smear; • The maternal and foetal risks from expectant
• Elevated liver enzymes; and a management (i.e. progression of hypertensive
• Low platelet count. disease and possible sequelae, including stillbirth
Patients with HELLP have a high risk of developing or asphyxia).
serious hepatic injury due to infarction, haemorrhage An overview of management of gestational hyperten-
and hepatic rupture. sion is beyond the scope of this chapter; however we
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will focus on the management of severe eclampsia in Table 49.4 Signs of magnesium toxicity
patients likely to need intensive care.
Serum magnesium Corresponding clinical
For the common scenarios where intensive care level (mmol/l) features
intervention is required, parenteral drug therapy for
3.5–5 Loss of deep tendon reflexes
acute management of severe hypertension is possible.
Labetolol intravenously is recommended for 5.0–6.5 Respiratory paralysis
first line therapy because it is effective, has a rapid >7.5 Cardiac conduction disturbances
onset of action and a good safety profile. Suggested >12.5 Cardiac arrest
regime: begin with 20 mg intravenously over 2 min-
utes followed at 10 minute intervals by doses of 20 to
80 mg up to a maximum total cumulative dose of 300 maintenance dose of 1 to 3 g/ hour. Intramuscular
mg, or an intravenous infusion of 1–2 mg/minute. regimes have been described but they are associ-
Hydralazine administered intravenously is a good ated with pain at the injection site and fluctuating
alternative to labetolol. Suggested regime: begin with drug levels. Magnesium sulphate is continued for 24
5 mg intravenously over 1 to 2 minutes, repeat as hours post partum. Therapeutic levels between 2.0
required waiting for a response that usually takes up and 3.5 mmol/l are to be maintained. Dose reduction
to 15–20 minutes to manifest. The maximum bolus might be needed in patients with renal failure. Clinical
dose is 20 mg. If a total dose of 30 mg does not achieve monitoring for signs of hypermagnesaemia, such as
optimal blood pressure control, another agent should reduced patellar reflexes and respiratory depression,
be used. should be monitored and the dose reduced if signs of
Calcium channel blockers, sustained release toxicity appear (Table 49.4).
nifedipine (30 mg) and immediate release nicardipine, Magnesium toxicity can be counteracted by
are other options. Nicardipine can be given intrave- administration of intravenous calcium chloride
nously. Experience with these drugs in pregnancy is 10 mmol slowly over 15–30 minutes.
limited. Immediate release oral or sublingual nifedi- Magnesium has a central effect in increasing sei-
pine is best avoided as it can cause precipitous hypo- zure threshold. The probable mechanisms of anticon-
tension resulting in uteroplacental insufficiency. vulsant action proposed are:
Nitroglycerin (glyceryl trinitrate) is a good option • NMDA receptor antagonism;
for treatment of hypertension associated with pulmo- • Non-specific calcium channel blockade, resulting
nary oedema. It is given as an intravenous infusion of in reduced release of acetyl choline at the
5 μg/minute and gradually increased every 3 to 5 min- postsynaptic motor nerve terminals;
utes to a maximum dose of 100 μg/minute. • Improved cerebral circulation by direct
Antenatal corticosteroids may also be adminis- antagonism of calcium mediated vasospasm.
tered. Neonatal respiratory distress is very common
in premature neonates of pre- eclamptic mothers. Invasive haemodynamic monitoring is useful in man-
Betamethasone should be administered to mothers aging these patients on the intensive care unit to help
<34 week’ gestation to promote foetal lung matura- monitor blood pressure, central venous pressure and
tion as the risk of these patients developing severe fluid status optimisation. The risk of bleeding due to
pre-eclampsia is high. thrombocytopenia should be considered whilst plac-
A ‘restrictive’ fluid strategy is advocated as patients ing these devices in patients.
with severe disease can develop pulmonary oedema.
Oliguria should be managed by modest trials of fluid Postpartum Care
boluses and if it does not respond it should be toler- A slow intravenous infusion of oxytocin (<2 U/min),
ated or renal replacement therapy considered if indi- which avoids systemic hypotension, is administered
cated. Pulmonary oedema might warrant use of loop after placental delivery to prevent maternal haem-
diuretics. orrhage. Prostaglandin F analogues are useful to
For seizure prophylaxis, magnesium sulphate is treat postpartum haemorrhage, unless an increase
the drug of choice and should be administered for in pulmonary artery pressure (PAP) is undesirable.
all patients with severe pre- eclampsia. Suggested Methyl-ergometrine is contraindicated because of the
regime: a loading dose of 4 to 6 g intravenously and risk (>10%) of vasoconstriction and hypertension.
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Meticulous leg care, elastic support stockings and or in the first 5 months after delivery without any
early ambulation are important to reduce the risk identifiable aetiology and with objective assessment
of thromboembolism. Delivery is associated with of left ventricular dysfunction. Risk factors associated
important haemodynamic changes and fluid shifts, with peripartum cardiomyopathy are maternal age
particularly in the first 12–24 hours, which may pre- older than 30 years, gestational hypertension and twin
cipitate heart failure, hence haemodynamic monitor- pregnancies. The aetiology is commonly a myocardi-
ing should therefore be continued for at least 24 hours tis or an autoimmune mechanism due to the presence
after delivery. of high serum titres of autoantibodies against human
cardiac tissue proteins. Ischaemic heart disease should
Amniotic Fluid Embolism be considered.
Amniotic fluid embolism (AFE) is an extremely rare Conventional heart failure management principles
but catastrophic event resulting in severe haemody- should be followed; however ACEI and angiotensin
namic collapse with disseminated intravascular coag- receptor blockers are contraindicated prior to delivery
ulation. It occurs when foetal cells, amniotic fluid and due to risk of impacting foetal growth. Amlodipine is
foetal hair enter the maternal circulation and incite an particularly beneficial in peripartum cardiomyopathy
inflammatory reaction similar to anaphylaxis. due to its anti-inflammatory nature.
Induction of labour, uterine rupture and polyhy- Mortality has reduced from approximately 7% to
droamnios are known risk factors. Most cases occur 2% with increased awareness and active management.
around the time of delivery, either vaginally or during Unlike traditional cardiomyopathies, cardiac function
caesarean sections (Table 49.5). normalises within 6 months post delivery in over 50%
Successful outcomes depend on early recognition, of patients suffering from the disease.
aggressive resuscitation and prompt delivery of the Subsequent pregnancies should be discouraged
baby within 5 minutes of commencing resuscitation. due to the high risk of recurrence, and if it occurs
Hysterectomy should be performed early if needed to should be managed at specialist obstetric units.
prevent major obstetric haemorrhage.
Suspected cases should be reported to UKOSS Hypertrophic Cardiomyopathy
(www.npeu.ox.ac.uk). Hypertrophic cardiomyopathy (HCM) is relatively
rare. Clinical deterioration during pregnancy is
Cardiomyopathy uncommon and it is determined by the degree of out-
flow tract obstruction. Baseline functional status is a
Peripartum Cardiomyopathy significant predictor of outcome.
Peripartum cardiomyopathy is defined as the develop- Management of HCM in pregnancy should focus
ment of heart failure in the last month of pregnancy on preventing blood loss and avoiding vasodilata-
tion. Beta- blockers, diuretics and calcium chan-
nel blockers are preferred to manage symptoms.
Implantation of an automatic defibrillator should
Table 49.5 Diagnostic criteria for amniotic fluid embolism be considered in patients with syncope or increased
Absence of a clear cause of acute maternal collapse with: arrhythmogenicity.
Acute foetal compromise Cardiac arrest Oxytocin is preferred over prostaglandins for
Rhythm disturbances Coagulopathy induction of labour. Vaginal delivery is preferred with
Hypotension Maternal haemorrhage
active management of second stage.
Seizure Shortness of breath
Excluding women with maternal haemorrhage as the first Congenital Heart Disease
presenting feature in whom there was no evidence of early The physiological changes of increased intravascular
coagulopathy or cardiorespiratory compromise volume, decreased systemic vascular resistance and
OR demand for increased cardiac output pose challenges
Women in whom the diagnosis was made at post mortem for patients with structural heart disease. These, along
examination with the finding of foetal squames or hair in the with the rapid fluid shifts during labour and delivery,
lungs
can precipitate heart failure.
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Maternal Risk Stratification hypertension limits appropriate adaptive responses

The modified WHO risk classification for maternal to the circulatory changes of pregnancy and to the
risk assessment has four classes: volatile changes during labour, delivery and the post-
Class I: Conditions with no detectable increase in partum period. These patients are also particularly
risk of maternal mortality and no/mild increase susceptible to pregnancy related complications such
in morbidity. For example, small patent ductus as pre-eclampsia, postpartum haemorrhage and pre-
arteriosus, mild pulmonic stenosis, mitral valve term delivery resulting in an extremely high mortality
prolapse. rate in the first postpartum week.
Class II: Small increase in risk of maternal If deemed necessary for a patient with class III or
mortality or moderate increase in morbidity. IV disease, the option of termination of pregnancy
For example unrepaired ventricular septal should be discussed and if the patient is willing this
defect, repaired tetralogy of Fallot, most should be performed in the first trimester of preg-
arrhythmias. nancy with a multidisciplinary team with surgical
Class III: Conditions are associated with significantly techniques. If medical techniques are to be used, mifo-
increased risk of maternal mortality or severe prostol (PGE1) is preferred. PGE2 and PGF should be
morbidity. For example mechanical valve, avoided.
systemic right ventricle, Fontan circulation,
bicuspid aortic valve with an enlarged ascending Management of Labour
aorta <50 mm and Marfan’s syndrome with an Supplemental oxygen therapy is always beneficial.
ascending aorta <45 mm. Oxytocin and mechanical methods (i.e. rupture of
Class IV: Conditions are associated with extremely membranes) is the preferred technique to induce
high risk of maternal mortality or severe labour. The parturient is nursed in the left lateral posi-
morbidity; pregnancy is contraindicated. For tion to relieve aortocaval compression. Pushing dur-
example severe mitral stenosis, symptomatic ing labour should not be encouraged as the raised
severe aortic stenosis, bicuspid aortic valve with intrathoracic pressure causes worsening of right to left
ascending aorta diameter >50 mm, Marfan’s shunt. The second stage should be assisted either with
syndrome with aorta dilated >45 mm, severe forceps or vacuum extraction.
systemic ventricular systolic dysfunction (left Preterm labour is a major concern because
ventricular ejection fraction <30%, New York immature foetuses are unlikely to be viable.
Heart Association [NYHA] III to IV), native Management of this scenario includes use of toco-
severe coarctation and significant pulmonary lytics such as salbutamol, which causes tachycardia
arterial hypertension of any cause (i.e. and can precipitate heart failure. Nifedepine and
pulmonary artery systolic pressure >25 mmHg indomethacin are preferred agents to arrest pre-
at rest or >30 mmHg with exercise). term labour.
Individual Risk Factors Caesarean delivery is reserved preferably for
The following are risks and predictors for maternal or obstetric indications, due to the additional risks of
foetal complications in women with congenital heart general anaesthesia, increased blood loss and postop-
disease during pregnancy: erative infections.
Oxytocin is the preferred uterotonic drug for
• Pulmonary hypertension (pulmonary vascular
postpartum use.
disease);
• Maternal cyanosis;
• Poor maternal functional class; Coronary Artery Disease in Pregnancy
• History of arrhythmia; Myocardial ischaemia in pregnancy is a relatively rare
• Maternal anticoagulants. occurrence, but the risk is higher during pregnancy
than in non-pregnant reproductive age women. Its
Pulmonary hypertension The most serious risk to incidence is expected to increase due to advancing
the mother is pulmonary hypertension, particu- maternal age and increased prevalence of risk factors
larly Eisenmenger syndrome, which includes the for coronary artery disease in the population. The
additional risk of maternal cyanosis. Pulmonary physiological changes of increased cholesterol, low
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415
density lipoprotein and triglycerides, and reduction in an abnormal rhythm. Sinus tachycardia is common-
high density lipoproteins during pregnancy contrib- est. The management of arrhythmia follows the gen-
ute. Diagnosis is established by conventional means of eral principles as for non-pregnant patients, but drug
ECG and cardiac enzyme analysis. therapy has to consider effects on the foetus and breast
Initial management consists of low dose aspirin feeding.
and beta-blockade due to their safety profile. Nitrates Table 49.6 gives a list of the common drugs used
and calcium channel blockers are to be used with cau- and their effects during pregnancy.
tion to prevent maternal hypotension. Thrombolysis
is a relative contraindication due to the risk of
antepartum haemorrhage. Both percutaneous trans- Deep Vein Thrombosis
luminal coronary angioplasty and coronary bypass Pregnancy is a prothrombotic state; due to stasis in the
graft surgery aiming to restore flow to the coronaries lower extremity caused by caval compression, there is
have favourable outcomes. Fluoroscopy and cinean an increase in vitamin K dependent clotting factors
giography times should be limited. The foetus should and a reduction in free protein S.
be shielded from direct radiation. The impact of this thromboembolic state is higher
The final trimester poses the highest risk due in patients with heart disease due to prosthetic valves,
to haemodynamic changes and the stress of labour. atrial arrhythmias and congenital heart disease with
Delivery is preferably delayed by 2–3 weeks after an cavopulmonary shunts.
acute MI with active management of labour to prevent Prophylactic anticoagulation with LMWH should
a prolonged second stage of labour. be continued and bridging anticoagulation regimes
with unfractionated heparin during labour or opera-
Cardiac Surgery with tive delivery should be commenced approximately 4–
6 hours prior to procedural intervention.
Cardiopulmonary Bypass
There is a significant risk of miscarriage and foetal
neurological impairment and foetal malformations Counselling and Genetic Testing
with cardiopulmonary bypass, though maternal Mothers with heart disease should be educated about
morbidity and mortality is similar to that of the non- the risks of pregnancy so that they can make an
pregnant population. The best period for surgery is informed decision. Patients with Eisemenger’s syn-
between the thirteenth-twenty eighth week. Before drome should be counselled against pregnancy and
surgery a full course (at least 24 hours) of corticos- if pregnant the option to terminate the pregnancy
teroids should be administered to the mother to aid should be discussed.
foetal lung maturation. During cardiopulmonary Children born to mothers with CVD have a high
bypass, foetal heart rate and uterine tone should be risk of developing cardiovascular disease, hence
monitored in addition to standard patient monitor- genetic testing may be useful, especially in cardio-
ing. Pump flow >2.5 l/min/m2 and perfusion pres- myopathies and channelopathies such as long QT
sure >70 mmHg are mandatory to maintain adequate syndrome. All women with congenital heart disease
blood flow into the pressure passive uteroplacental should be offered foetal echocardiography in the sec-
bed. Maternal haematocrit >28% is recommended to ond trimester, and a chorionic villous biopsy around
optimise the oxygen delivery. Normothermic perfu- 12 weeks of gestation if indicated.
sion, when feasible, is advocated, and state of the art
pH management is preferred to avoid hypocapnia
responsible for uteroplacental vasoconstriction and Learning Points
foetal hypoxia. Cardiopulmonary bypass time should • Pregnancy causes complex alterations in
be minimised. cardiovascular physiology and the changes tend
to persist for about 2 weeks into the postpartum
Arrhythmias in Pregnancy period.
Palpitation is a very common symptom during preg- • A single diagnostic investigation requiring
nancy especially in structurally abnormal hearts; about radiation exposure does not threaten the well
50% of Holter monitoring recordings demonstrate being of the developing foetus.
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Table 49.6 Antiarrhythmic drugs used in pregnancy
Drug Safety in Safety in Comments

pregnancy breastfeeding
Class I
Quinidine Safe Safe Can precipitate premature labour
Procainamide Safe Safe Can cause lupus like syndrome, agranulocytosis
Lidocaine Safe Safe Toxicity can cause foetal distress
Flecainide Safe Unknown Has been used, no significant complications reported
Class II: Beta-blockers
Atenolol Unsafe Safe Avoid atenolol in first trimester as can cause IUGR
Class III
Amiodarone Safe Unsafe For short term emergency use
Can cause IUGR, goitre, foetal hypo/hyperthyroidism
Class IV: Calcium channel blockers
Verapamil Safe Safe
Diltiazem Unsafe Unknown IUGR, skeletal anomalies, foetal death
Adenosine Safe Safe Lesser dose needed as degradation is slower in pregnancy
Digoxin Safe Safe Can cause miscarriage and foetal death at toxic levels
Atropine Unknown Unknown Used in resuscitation
All antiarrhythmic drugs cross the uteroplacental barrier
• ECMO should be considered as an option to diagnosis, and medical and surgical management.
manage amniotic fluid embolism. Canadian Journal of Cardiology. 2010; 26:
• Pulmonary hypertension is a serious risk factor in e185–189.
pregnancy as it limits the cardiovascular system to Magee LA, Pels A, Helewa M, Canadian Hypertensive
mount appropriate adaptive responses to pregnancy Disorders of Pregnancy (HDP) Working Group, et al.
The hypertensive disorders of pregnancy (29.3). Best
and labour with a very high rate of mortality in the
Practice & Research: Clinical Obstetrics & Gynaecology.
first week of the peripartum period. 2015; 29: 643–657.
• All antiarrthymic drugs cross the uteroplacental
Regitz-Zagrosek V, Gohlke-Bärwolf C, Iung B, Pieper
barrier and careful consideration should be given PG. Management of cardiovascular diseases during
to the effects on the foetus. pregnancy. Current Problems in Cardiology. 2014;
39: 85–151.
Further Reading Regitz-Zagrosek V, Lundqvist CB, Borghi C, et al. ESC

Guidelines on the management of cardiovascular
ACOG Committee. Opinion #299: Guidelines for diseases during pregnancy. European Heart Journal.
diagnostic imaging during pregnancy. Obstetrics & 2011; 32: 3147–3197.
Gynecology. 2004; 104(3). Savu O, Jurcuţ R, Giuşcă S, et al. Morphological and
Diller G-P, Dimopoulos K, Okonko D, et al. functional adaptation of the maternal heart during
Exercise intolerance in adult congenital heart pregnancy. Circulation: Cardiovascular Imaging.
disease: comparative severity, correlates, and 2012; 5: 289–297.
prognostic implication. Circulation. 2005; Siu SC, Sermer M, Colman JM, et al. Prospective
112: 828–835. multicenter study of pregnancy outcomes in
Honigberg MC, Givertz MM. Arrhythmias in peripartum women with heart disease. Circulation. 2001;
cardiomyopathy. Cardiac Electrophysiology Clinics. 104: 515–521.
2015; 7: 309–317. Tuffnell D, Knight M, Plaat F. Amniotic fluid embolism –
Kealey AJ. Coronary artery disease and myocardial an update. Anaesthesia. 2011; 66: 3–6.
infarction in pregnancy: a review of epidemiology,
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Weiss BM, von Segesser LK, Alon E, Seifert B, Turina MI. American Journal of Obstetrics and Gynecology. 1998;
Outcome of cardiovascular surgery and pregnancy: a 179: 1643–1653.
systematic review of the period 1984–1996.
MCQs
1. Cardiovascular disease in pregnancy: (d) Liberal fluid infusions are the mainstay of treat-
(a) Is increasing in prevalence ment for reduced urine output
(b) Valvular heart disease is commonest (e) Does not present post partum
(c) Congenital heart disease has the highest prevalence 4. Peripartum cardiomyopathy:
in cardiovascular disorders in pregnancy (a) Is unlikely to be diagnosed post partum
(d) There are multiple large cohort trials guiding man- (b) Has a mortality of 30% at 1 year
agement of cardiovascular disease in pregnancy (c) Angiotensin converting enzyme inhibitors are the
(e) Complex congenital heart disease in pregnancy is mainstay of treatment during pregnancy
best managed in the community (d) Unlike pre-eclampsia, twin pregnancy is not a
2. Cardiovascular physiology in pregnancy: risk factor
(a) Anaemia in pregnancy is a result of decreased red (e) Further pregnancies should be discouraged as there
cell mass is a high incidence of recurrence
(b) Systemic vascular resistance increases 5. Diagnostics of cardiovascular disease in pregnancy:
(c) Systolic blood pressure decreases from early (a) A radiation dose below 50 mGy to the pregnant
pregnancy mother is the accepted level of radiation below
(d) Aortocaval compression by the uterus can be seen which there is no evidence of increased foetal risk
from the second trimester (b) Gadolinium ions are known to cross the placental
(e) Cardiac output increases post partum barrier
3. Pre-eclampsia: (c) Amniotic fluid embolism is an extremely rare but

catastrophic event resulting in severe haemody-
(a) Is diagnosed if systolic blood pressure is over namic collapse with disseminated intravascular
120 mmHg coagulation
(b) Is diagnosed if proteinuria is present (d) Echocardiography is the preferred mode of imaging
(c) Home blood pressure monitoring is not a diagnos- of the heart in pregnancy
tic tool; it needs to be measured in hospital (e) All of the above
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Section 7
Chapter
Paediatric Cardiac Intensive Care
50 Ajay Desai, Lidia Casanueva and Duncan Macrae
Introduction the physiology of congenital heart disease is key to its

successful management in critical care.
Cardiovascular disorders are common in critically ill
For neonates, as a rule of thumb, mean arte-
children, accounting for around 30% of the UK annual
rial blood pressure for term (40 weeks’ gestation) is
total of 20,000 paediatric critical care unit admissions.
40 mmHg, and proportionately lower with increased
Of these children, over 60% were under 1 year of age
prematurity.
and 83% under 5 years of age on admission.
Assessment of the Circulation in Congenital Heart Disease

The incidence of congenital heart disease (CHD) is
Children widely stated to be 8 per 1000 live births. Although
Assessment of the circulation in children must rates vary, from region to region, up to 60% of babies
include both a rapid ‘ABC’ safety assessment (Is the with a congenital heart problem are identified antena-
airway clear? Is the child breathing adequately? Is tally. This is important as an appropriate plan for the
there a pulse?), and then a more detailed examination. care of the newborn infant can be established before
A child’s appearance is a good guide to their overall birth. In the absence of antenatal detection, many
state of wellness. Are they moving normally for their babies with CHD present either immediately after
age? Are they lethargic or lacking interest in parents birth or within the first weeks of life. The mode of
or staff? Are they restless or inconsolable (cerebral presentation depends greatly on the nature and sever-
hypoxia)? What do the parents think? Assessing work ity of the heart defect, and a structured approach to
of breathing (WOB) is another important part of the neonate with CHD is required.
cardiorespiratory assessment, as it will be increased
in the presence of pulmonary oedema which reduces
lung compliance. The respiratory rate, the presence Approach to the Neonate with
of grunting (indicating attempts to maintain lung Suspected CHD
recruitment), and the presence of intercostal and
subcostal retractions, tracheal tug and head bobbing, Common Presentations
which all indicate a child has significantly increased
WOB, should be observed. Skin perfusion should Cyanosis
be assessed by determining capillary refill time (<3 Persisting cyanosis after initial resuscitation at birth
seconds after 5 seconds of pressure). Blood pressure, must be rapidly assessed and managed. The evaluation
heart rate, respiratory rate and SpO2 should always should assess the infant for airway, pulmonary and
be measured as part of the child’s initial admission circulatory causes of cyanosis, using a logical ABC
assessment and at appropriate intervals thereafter, algorithm (see Table 50.2).
taking into account age related normal values (see In the absence of major airway or breathing prob-
Table 50.1) and in the case of SpO2, the expected satu- lems, neonatal cyanosis is most likely to be due to
ration values for the child’s pathology. Understanding CHD or persistent pulmonary hypertension of the
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Chapter 50: Paediatric Cardiac Intensive Care
Table 50.1 Normal values for heart rate and blood pressure in children
Age of child (years)

<1 1–2 2–5 5–12 >12
Respiratory rate 30–40 25–35 25–30 20–25 15–20
Heart rate 110–160 100–150 95–140 80–120 60–100
Systolic blood pressure 80–90 85–95 85–100 90–110 100–120
Table 50.2 Common causes of severe cyanosis in the neonate
Airway Breathing Circulation

Tracheal anomalies Pneumonia CHD with decreased pulmonary blood flow
• Tracheal stenosis • Pulmonary atresia
• Vascular compression • Tetralogy of Fallot
• Tricuspid atresia
• Ebstein’s anomaly
Choanal atresia Congenital lung anomalies CHD with diversion of blood
• Remember neonates are obligate • Diaphragmatic hernia • Transposition of the great arteries
nose breathers • Pulmonary hypoplasia
• Congenital lobar emphysema
Vocal cord paralysis Phrenic nerve palsy Persistent pulmonary hypertension of the newborn
• May occur in isolation or in association with sepsis,
meconium aspiration or other lung anomalies
Central hypoventilation
newborn (PPHN), which may occur with or without includes oxygen therapy and the administration of
clear triggers. alprostadil (prostaglandin E1) or dinoprostone (pros-
At birth, important changes in cardiovascular and taglandin E2) to re-establish patency of the arterial
respiratory systems must occur for infants to adapt duct, which permits flow of blood from the aorta to
adequately to extrauterine life. In the foetus pulmo- the pulmonary artery. This will not cause harm even if
nary blood flow remains low due to a high pulmonary the cause of the cyanosis is PPHN. Urgent evaluation
vascular resistance. At birth as the lungs fill with air, will include chest X-ray, ECG, and echocardiogram
pulmonary vascular resistance should fall rapidly with and a hyperoxia test.
an 8- to 10-fold rise in pulmonary blood flow ensur- If CHD with obstructed pulmonary blood flow is
ing adaption to pulmonary oxygenation of blood. If confirmed, prostaglandin infusion should continue
factors such as meconium aspiration are present, pul- until a more definitive pulmonary blood supply is
monary vascular resistance may not fall normally, a established through surgical or cardiological inter-
physiological state described as PPHN. Right to left vention. Care should be taken to ensure that prosta-
shunting of blood then continues through foetal chan- glandins E1 and E2 are infused at the lowest effective
nels (the foramen ovale and arterial duct) resulting in dose, as dose related apnoeas are common at doses
systemic cyanosis. >10 ng/kg/minute. Usual starting doses are 5–10 ng/
Cyanosis due to congenital heart disease occurs in kg/minute; maximum recommended dose for both
broad groups of anomalies: firstly those anomalies in drugs is 100 ng/kg/minute.
which there is obstruction to blood flow to the lungs
such as pulmonary atresia and critical pulmonary ste- Cardiogenic Shock
nosis, and secondly conditions in which oxygenated Neonates may also present at birth or in the early
blood does not reach the systemic circulation. neonatal period with shock. The differential diag-
Immediate management of the neonate with nosis includes sepsis, metabolic disorders, arrhyth-
suspected cyanotic CHD and adequate breathing mias and structural cardiovascular disease. Common
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structural heart conditions presenting as shock soon Initial management of infants presenting with
after birth include critical aortic stenosis, aortic coarc- heart failure, following a rapid ‘ABC’ assessment, is to
tation and hypoplastic left heart syndrome (HLHS), start diuretics (frusemide ± spironolactone) and pos-
all of which result in circulatory decompensation sibly an ACE inhibitor (captopril). Oxygen therapy
when the arterial duct closes. Decompensated babies should be avoided unless the baby presents with cya-
with aortic coarctation or interrupted aortic arch clas- nosis, as higher inspired oxygen fractions will further
sically present in shock due to minimal descending lower pulmonary vascular resistance and may worsen
aortic blood flow, with raised plasma lactate, weak cardiac failure. Nasal or facial CPAP or BiPAP is effec-
or absent femoral pulses and right upper limb hyper- tive in off-loading the left ventricle and is an effective
tension. A standard ABC approach to evaluation and adjunct to diuretics in the acutely decompensated
resuscitation should be adopted and, as with cyanotic babies with left or congestive heart failure.
lesions, a prostaglandin E1 or E2 infusion should be
started even if the definitive diagnosis has not been Arrhythmia
established. Care should be taken to minimise FiO2 in Babies may develop arrhythmia in utero to the extent
babies with HLHS and other ‘single ventricle’ lesions, that they are compromised before, during and after
as inadvertent lowering of pulmonary vascular resist- birth. Congenital complete heart block may be rela-
ance by generous oxygen therapy risks diverting blood tively well tolerated, or may be associated with foetal
away from the systemic circulation (Qs) by increasing hydrops, critically low cardiac output and multiorgan
pulmonary blood flow (Qp). failure. Adrenaline or isoprenaline infusions may be
used to increase heart rate temporarily until definitive
Pulmonary Oedema cardiac pacing is established.
Neonates with obstructed total anomalous pulmonary Tachyarrhythmias commonly presenting at birth
venous drainage (TAPVD) may present with severe include atrial flutter and supraventricular tachycar-
dyspnoea, hypoxia and circulatory collapse soon dia. Neonates may be severely shocked as a result of
after birth. Chest X-ray will show severe pulmonary fast rhythms and require urgent treatments including
oedema. Non-cardiac causes of neonatal cardiorespi- cardioversion (atrial flutter), intravenous bolus aden-
ratory failure must be rapidly ruled out, and echocar- osine (converts or permits diagnosis by transient slow-
diographic examination obtained urgently, although ing of heart rate in SVT) and intravenous amiodarone
TAPVD can be challenging to diagnose, especially in (slows/facilitates return to sinus rhythm in a variety of
critically ill ventilated babies. supraventricular and ventricular tachycardias).
Other congenital heart lesions also present with
pulmonary oedema (see below), although the severity
of pulmonary oedema is initially less, and the onset of
Postoperative Care of the Child Following
milder symptoms is more gradual, starting at the age Cardiac Surgery
of several weeks or months, rather than at or within Cardiopulmonary bypass in neonates and young
days of birth. children frequently results in a clinically important
systemic inflammatory response causing important
Heart Failure and Failure to Thrive organ assistant dysfunctions including myocardial
Infants with several common congenital heart lesions, depression, acute kidney injury and a loss of capillary
such as ventriculoseptal defect (VSD), atrioventricu- integrity leading to generalised extravascular fluid
loseptal defect (AVSD), large atrial- septal defects accumulation.
(ASD) and rarer conditions such as truncus arterio- Low cardiac output frequently occurs following
sus and aortopulmonary window, gradually develop cardiac surgery. Common causes include hypovolae-
congestive cardiac failure as their pulmonary vascular mia, myocardial depression and the effects of resid-
resistance gradually falls over the first weeks of life. ual cardiac defects and arrhythmias. A structured
This often presents as tachypnoea, hepatomegaly and approach to the management of low cardiac output is
failure to thrive. The chest X-ray usually demonstrates shown in Figure 50.1. As well as clinical and haemo-
cardiomegaly and signs of increased pulmonary blood dynamic assessment including ECG, careful echocar-
flow. Echocardiographic examination is required to diograph examination should be undertaken to assess
establish the definitive diagnosis. the integrity of the cardiac repair, detect the presence
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LOW CARDIAC OUTPUT STATE
Fluid restriction Fluid challenge 5–10 ml/kg

Diuretic HIGH LOW Blood if haematocrit < 0.4
Preload Reassess and repeat if needed
Venodilator
Beware of bleeding (check Hb)
Volume status adequate?

Sedation/analgesia adequate?
Hyperthermia? Obtain 12-lead ECG, determine rhythm
Obtain 12-lead ECG, determine rhythm Consider:
HIGH LOW - Anticholinergics
Consider: Heart rate
- Electrolytes
- Antiarrhythmics
- Pacing
- Electrolytes
- Isoproterenol (0.05–2 µg/kg/min)
- Cooling
- Overdrive pacing
- DC cardioversion
Blood pressure
HIGH or
NORMAL LOW
Vasodilator Inotrope
Nitroglycerin 1–5 µg/kg/min Epinephrine 0.01–0.05 µg/kg/min

or Inodilator or
Nitroprusside 1–8 µg/kg/min Dobutamine 5–15 µg/kg/min
Milrinone or
Load + 0.25–0.75 µg/kg/min (Dopamine 3–10 µg/kg/min)
Epinephrine 0.06–0.5 µg/kg/min

± vaso/inodilator
Mechanical circulatory support
(ECMO/VAD)
Aiming for recovery of native heart or
bridging for cardiac transplantation
Norepinephrine 0.05–1 µg/kg/min
Consider vasopressin for severe

Consider adjunctive treatment strategies hypotension associated with low
(calcium, corticosteroid, thyroxine) vascular resistance
In refractory cases consider levosimendan
In associated PHT consider iNO, sildenafil,

prostacyclin, bosentan
Figure 50.1 Management of a child with low cardiac output state.

Assess Airway, Breathing and Circulation:
• Consider underlying physiology –univentricular versus biventricular circulation
• Correct hypoxia, acidosis, hyperthermia and electrolyte imbalance
• Look for tamponade, residual or unsuspected anatomical or physiological abnormality –perform echocardiography
• Consider need for respiratory support –non-invasive or invasive –beware of vasodilatation and myocardial depression of
anaesthesia drugs.
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422
of any residual lesions, provide information on ven- over-distension all act to minimise PVR. Acidosis,
tricular contractility to guide therapy, and to identify both metabolic and respiratory, and pain also cause
pericardial effusion as a cause of the low output state. PVR to rise. Whilst induced alkalosis is not recom-
mended for the prevention of PHT, brief periods of
hyperventilation to lower pCO2 and raise pH, thereby
Tamponade and Delayed Sternal lowering PVR, can be successful in controlling sud-
Closure den dangerous rises in PAP/PVR. The aim should be
In children as in adults, haemorrhagic pericardial tam- to maintain normal pH and avoid acidosis and inad-
ponade can cause major haemodynamic instability equate pain relief, which will act to raise PVR/PAP.
following cardiac surgery. Haemorrhagic tamponade Inhaled nitric oxide (iNO) is a specific pulmo-
must be actively prevented by careful surgical haemo- nary vasodilator and can be extremely effective in
stasis and normalisation of coagulation. Tamponade lowering PAP/ PVR in the postoperative period.
must be actively excluded in patients who continue Phosphodiesterase 5 inhibitors such as sildenafil may
to bleed or who develop unexplained cardiovascular be used as an adjunct to iNO acutely, or for longer
instability following surgery. In neonates and young term pulmonary vasodilatation. Endothelin receptor
children, tissue oedema resulting from the systemic blockers and prostacyclin are also effective pulmonary
inflammatory response may result in swelling of the vasodilators most useful in longer term management.
intrathoracic organs and consequent pressure on the
heart with similar effects to haemorrhagic tampon-
ade. For this reason, many surgeons choose to delay
Univentricular Circulations
Some congenital heart lesions are so severe that it is
sternal closure thereby decompressing the thorax
not possible to repair the heart to create two function-
and preventing this complication. The sternum can
ing ventricles. An extreme example of this is hypo-
then be formally closed a few days following surgery
plastic left heart syndrome (HLHS) in which all of the
once haemodynamic stability is achieved and tissue
left heart structures, including the left ventricle, mitral
oedema has subsided.
valve, aortic valve and ascending aorta, are extremely
small. If only one useful ventricle exists, or if the two
Pulmonary Circulation and Pulmonary ventricles cannot be partitioned, the ventricle(s) must
Hypertension be assigned to the systemic circulation and pulmo-
nary blood flow secured initially with a systemic-
Understanding of the physiology and pharmacol-
pulmonary artery shunt (modified Blalock–Taussig
ogy of the right ventricle and pulmonary circulation
shunt) or temporary ventricle-pulmonary artery con-
are crucial to the good management of children with
duit. The aim of this initial palliation is to enable the
congenital heart disease. A low pulmonary vascu-
child to grow, and also allow time for the natural post-
lar resistance (PVR) is necessary when congenital
natal fall in pulmonary vascular resistance to occur,
heart lesions require cavopulmonary connections
as low PVR is essential for progression down the ‘uni-
(see below). Children with uncontrolled pulmonary
ventricular’ pathway.
blood flow from large left-to-right shunts, and those
with obstructed pulmonary venous drainage or very
high systemic atrial pressures are at risk of develop- Initial Palliation of the Univentricular Circuit
ing muscularisation of pulmonary arterioles, raised In neonates with systemic-pulmonary artery shunts,
PVR and high pulmonary artery pressures (PAP). The the pulmonary and systemic circulations are both
inflammatory response to CPB may cause temporary fed by the systemic ventricle. The flow of blood to the
elevations in PVR or increased pulmonary vascular lungs is limited by the resistance of the shunt, and also
reactivity requiring interventions to lower PVR and the pulmonary vascular resistance. The systemic blood
PAP, as failure to do so will result in acute right ventri- flow is determined by any anatomical factors (e.g.
cle failure with secondary left ventricular failure and residual aortic obstruction) and the systemic vascular
cardiovascular collapse. resistance (SVR). The balance of these factors deter-
Simple measures to ensure low PVR include careful mines the balance of blood flow between the systemic
pulmonary management. Maintaining lung recruit- and pulmonary circuits. If PVR is low and the Blalock
ment, avoiding alveolar hypoxia whilst avoiding lung shunt is large, pulmonary blood flow will be excessive
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at the expense of systemic blood flow. Postoperatively, doing so loss of lung volume through failure to apply
intensivists may have to intervene, particularly with adequate PEEP must also be avoided. Hypovolaemia
measures to raise the lower PVR or SVR to achieve is poorly tolerated in cavopulmonary patients, as it is
the required balanced circulation. Measurement the hydraulic gradient across the lungs, which drives
of the saturation of blood in the superior vena cava blood from the SVC to the systemic atrium. Arterial
and the arterial blood enable a crude estimate of the saturations after a Glenn shunt are usually in the 80–
Qp:Qs ratio to be determined, the aim being a ratio 85% range. Saturations below 75% are inadequate and
of 1:1 which, with normal cardiac output and oxygen require careful investigation to determine the cause,
extraction, typically results in a systemic saturation of which might include compromise of the surgical
75–80%. High saturations (>85%) in shunted babies shunt or elevated PVR.
strongly suggest excessive Qp (Qp:Qs > 1). Babies
with unexpectedly low saturations after shunt proce-
dures may have high PVR and/or low cardiac output
Total Cavopulmonary Connection
but must always be investigated for shunt patency and The final stage of palliation for ‘single ventricle’ cir-
function: is the shunt blocked? Is the shunt too small culations is the completion of the cavopulmonary
or compromised in some way? pathway by connecting inferior vena caval blood to
the pulmonary artery in what is often referred to as
a ‘Fontan completion’ or total cavopulmonary con-
Superior Cavopulmonary Connection nection’ (TCPC) operation. This is typically done in
At around 4–6 months of age, babies with palliated early childhood and results in normal or near nor-
(i.e. shunted) univentricular circulations typically mal systemic oxygenation despite the presence of
undergo a superior cavopulmonary connection or only one effective ventricle. Post procedure, Fontan
‘bi-directional Glenn’ procedure. In this operation the patients tolerate hypovolaemia or factors raising PVR
SVC is disconnected from the atrium and anastomo- poorly, as blood must flow passively across the lungs
sed to a central pulmonary artery. SVC return now driven by central venous/pulmonary artery pressure
flows directly to the lungs without any cardiac assist. alone. Early postoperative hypotension in Fontan
For this ‘cavopulmonary’ circulation to succeed, the patients usually responds well to volume augmenta-
baby must have a low PVR and the systemic ventricle tion although care should also be taken to ensure that
must function well and specifically have a competent ventricular function is adequate, and the ventricle
systemic AV valve, and low systemic atrial pressure. supported appropriately with inotropes if required.
After a Glenn shunt, the SVC pressure is the upstream
pulmonary artery pressure, whilst the systemic atrial Mechanical Circulatory Support in
pressure, directly measured or inferred from meas-
urement of femoral vein pressure, gives the transpul-
Children
Mechanical circulatory support, usually venoarterial
monary pressure gradient (TPG). A TPG gradient of
ECMO, plays an important role in the management
<10 mmHg is entirely satisfactory, typically giving a
of children with very severe circulatory failure in the
PA/SVC pressure of 12–15 mmHg (TPG + systemic
cardiac intensive care unit. Indications include:
atrial pressure). Pulmonary blood flow is maximised
by reducing the mean intrathoracic pressure gener- • Failure to separate from intraoperative
ated by positive pressure ventilation. Spontaneous cardiopulmonary bypass;
breathing improves venous return to the thorax and • Severe postoperative low cardiac output
should be encouraged as early as possible in postop- syndrome;
erative children with cavopulmonary circulations. • Cardiac arrest not responding promptly to
Alkalosis, easily induced by injudicious hyperventila- standard resuscitation;
tion, has been shown to reduce flow in the superior • Severe heart failure as a bridge to transplantation
cavopulmonary shunt as a result of cerebral vasocon- or recovery.
striction. Positive pressure ventilation in children with Several key factors are important in achieving good
superior cavopulmonary connections should there- outcomes from paediatric cardiac ECMO support.
fore be carefully delivered to avoid excessive intratho- ECMO is a complex and costly technique, and should
racic pressure and respiratory alkalosis, although in only be considered when children are not responding
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adequately to conventional support measures. Its possible by echocardiogram, and re-exploration of

deployment must be timely, and not delayed beyond the chest to evacuate clot and secure haemostasis.
the point where recovery of the heart or other organs Cardiac tamponade can also occur in children,
is no longer probable. Perioperative support should especially neonates and infants, who may develop a
be considered in children with severe but potentially significant inflammatory response following CPB,
recoverable myocardial dysfunction, or where bridg- resulting in swelling of tissues including the intratho-
ing to cardiac transplantation, perhaps with later racic organs and tissues resulting in ‘tissue tampon-
implantation of a long-term ventricular assist device, ade’. To prevent tissue tamponade, surgeons can elect
is possible. to delay sternal closure, stenting the two sides of the
Several technical aspects are necessary to achieve sternum apart, undertaking closure once the inflam-
excellent outcomes. Good ECMO cannula position matory response has ebbed and cardiovascular stabil-
is key to obtaining ECMO flows and therefore organ ity is assured.
system support. Cardiac decompression lowers myo-
cardial oxygen consumption, facilitating myocardial
recovery, and decompresses the systemic atrium,
Arrhythmia
preventing pulmonary oedema or haemorrhage, and Common arrhythmias following cardiac surgery in
must be assured at the initiation of ECMO. Left (or children include slow and fast rhythms.
systemic) atrial decompression can be achieved in a Slow Rhythms
number of ways including supplementary direct left
There is a higher risk of partial or complete AV block
atrial cannulation or percutaneous creation of an
during surgery on or near the ventricular septum or
interatrial communication. Bleeding is particularly
AV node. Complete AV block requires AV sequen-
challenging during cardiac extracorporeal life support
tial pacing at an appropriate rate via temporary atrial
(ECLS) in postoperative children. Meticulous surgical
and ventricular wires. Sinus rhythm may return but,
haemostasis and cannulation, together with careful
beyond 10 days, implantation of a permanent pacing
monitoring of heparin administration, and clotting
system is indicated.
parameters, must be ensured.
International figures show that approximately Fast Rhythms
40% of children receiving cardiac ECMO survive to
Junctional ectopic tachycardia (JET or His bundle tach-
ICU discharge. Acute fulminant myocarditis, once
ycardia) occurs relatively commonly in children fol-
considered a fatal disease, is associated with 60–80%
lowing surgery near the conducting system. Typically
chance of myocardial recovery with ECMO support.
this rhythm ‘warms up’, that is the heart rate gradually
Conversely, patients with single ventricle physiology,
rises as P waves become indistinct. Classically, the ECG
especially those supported after the Norwood pro-
will show that the ventricular rate exceeds the atrial
cedure, have relatively poor outcomes, with 20–25%
rate with AV dissociation. Cardiac output is usually
chance of survival to PICU discharge.
compromised in fast rhythms, and measures to control
ELSO have published standards, training material
the rate usually include: (i) inducing moderate hypo-
and supported many publications to which interested
thermia (34–35 °C) to slow the ventricular rate and/
readers are referred (www.elso.org).
or intavenous amiodarone, (ii) atrial or AV sequential
pacing once the ventricular rate has slowed sufficiently.
Common Complications JET resolves after several days. Long-term antiarrhyth-
mic control is not usually required.
Bleeding Atrial fibrillation and malignant ventricular
The management of bleeding following cardiac sur- rhythms, although seen occasionally, are far less com-
gery in children differs little from that in adults. mon following cardiac surgery in children than in
adults.
Cardiac Tamponade
The occurrence of and management of haemorrhagic Residual Lesions
pericardial tamponade is managed as in adults: Despite the best efforts of cardiologists and surgeons,
timely detection on clinical suspicion, confirmed if children may fail to progress smoothly following
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425
surgery due to residual lesions. Any child whose post- results from accumulation of lymph- rich pleural
operative course deviates from the expected course effusions due to overspill as the lymphatic system is
must be urgently re-evaluated clinically, further imag- overloaded, or lymphatic drainage is impeded by high
ing undertaken (echocardiography, cardiac CT, CMR) systemic venous pressures (often seen in cavopulmo-
and where indicated cardiac catheterisation performed. nary circulations) of venous thrombosis.
Chylothorax is managed by diagnosing that the
Acute Kidney Injury effusion is indeed chylous (white cells of fluid >85%
lymphocytes). A potential cause for the problem
Transient perturbation of renal function is relatively
should be sought, and adverse factors corrected if pos-
common in neonates and young infants following
sible, or reoperation is required if the loss is clearly
cardiac surgery on CPB, and in any sick child with
surgical in origin. Medical management includes as a
critically low systemic perfusion. Peritoneal dialysis
first step, a diet severely limiting long chain fatty acids,
is very effective in providing renal replacement ther-
replacing these with medium chain fats which are not
apy (RRT) in this age group. Although rarely needed,
transported by the lymphatic system. Further steps to
RRT in older children is undertaken using continuous
reduce chyle production include nil-by-mouth with
venovenous haemofiltration.
total parenteral nutrition and low-dose vasopressin
infusion. If chylous effusions persist long-term, con-
CNS sideration should be given to performing a surgical
Transient seizures or brain imaging anomalies are sur- pleuradhesis.
prisingly common in neonates and infants before and
after cardiac surgery. Whilst their prognosis is gener-
ally good, children with minor problems require close Learning Points
neurodevelopmental follow-up, whilst children devel- • Immediate management of the neonate with
oping infarcts, hypoxic ischaemic encephalopathy or suspected cyanotic CHD and adequate breathing
intracranial bleeds require multidisciplinary postop- includes oxygen therapy and the administration
erative management and specialist follow-up. of prostaglandin E1 or E2. There are no absolute
contraindications to initiate prostaglandin
Phrenic Nerve Injury and Diaphragmatic therapy, although it may worsen the pulmonary
oedema associated with obstructed total
Paralysis anomalous pulmonary venous return.
The phrenic nerves run across the pericardium and • Low cardiac output syndrome (LCOS) affects
may be injured or transected during cardiac surgery up to 25% of neonates and young children after
resulting in temporary or permanent paralysis of the cardiac surgery. Residual cardiac lesions, even
associated hemidiaphragm. Paralysis of one hemidia- when minor, may also adversely impact the
phragm is well tolerated in most adults and in children postoperative course.
over 2 years of age. Neonates and infants do not have a • Postoperative complete atrioventricular block, if
well-developed intercostal-rib inspiratory system, and it persists beyond 10 days, indicates implantation
often fail to separate from mechanical respiratory sup- of a permanent pacing system.
port in the presence of a paralysed hemidiaphragm. • Hypovolaemia is poorly tolerated in
Undertaking plication of the hemidiaphragm stabi- cavopulmonary patients. After a Glenn shunt,
lises the base of the thorax, preventing paradoxical a transpulmonary pressure gradient (TPG) of
displacement of the affected lung during inspiration, <10 mmHg is satisfactory, typically giving a PA/
improving inspiratory efficiency to a sufficient degree SVC pressure of 12–15 mmHg.
to facilitate ventilator weaning. • The ICU survival rates are approximately 40% for
children receiving cardiac ECMO. Whilst the ICU
Chylous Effusions and Chylothorax survival rates are relatively poorer (20–25%) for
Postoperative chylothorax in its ‘pure’ form results single ventricle physiology patients supported on
from damage to a major lymphatic vessel at surgery, ECMO, the chances of myocardial recovery on
resulting in chyle accumulating in the affected pleural ECMO support are better for patients with acute
space. More commonly what is termed ‘chylothorax’ fulminant myocarditis (60–80%).
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Further Reading Li S, Krawczeski CD, Zappitelli M, for the TRIBE-AKI

Consortium. Incidence, risk factors, and outcomes of
Barr FE, Macrae D. Inhaled nitric oxide and related acute kidney injury after pediatric cardiac surgery: a
therapies. Pediatric Critical Care Medicine. 2010; 11(2 prospective multicenter study. Critical Care Medicine.
Suppl): S30–S36. 2011; 39: 1493–1499.
Brunner N, de Jesus Perez VA, Richter A, et al. Panthongviriyakul C, Bines JE. Post-operative chylothorax
Perioperative pharmacological management of in children: an evidence-based management algorithm.
pulmonary hypertensive crisis during congenital heart Journal of Paediatrics and Child Health. 2008;
surgery. Pulmonary Circulation. 2014; 4: 10–24. 44: 716–721.
Chaturvedi RR, Macrae D, Brown KL, et al. Cardiac ECMO Penny DJ, Shekerdemian LS. Management of the neonate
for biventricular hearts after paediatric open heart with symptomatic congenital heart disease. Archives of
surgery. Heart. 2004; 90: 545–551. Disease in Childhood. Fetal and Neonatal Edition. 2001;
Friedman AH, Fahey JT. The transition from fetal 84: 141–145.
to neonatal circulation: normal responses and Talwar S, Patel K, Juneja R, Choudhary SK, Airan B. Early
implications for infants with heart disease. Seminars in postoperative arrhythmias after pediatric cardiac
Perinatology. 1993; 17: 106–121. surgery. Asian Cardiovascular and Thoracic Annals.
Hallidie-Smith KA. Prostaglandin E1 in suspected ductus 2015; 23: 795–801.
dependent cardiac malformation. Archives of Disease in Tibby SM, Brock G, Marsh MJ, et al. Haemodynamic
Childhood. 1984; 59: 1020–1026. monitoring in critically ill children. Care of the
Hoskote A, Li J, Hickey C, Erickson S. The effects of Critically Ill. 1997; 13: 86–89.
carbon dioxide on oxygenation and systemic, cerebral, Wernovsky G, Wypij D, Jonas RA, et al. Postoperative
and pulmonary vascular hemodynamics after the course and hemodynamic profile after the arterial
bidirectional superior cavopulmonary anastomosis. switch operation in neonates and infants: a comparison
Journal of the American College of Cardiology. 2004; of low-flow cardiopulmonary bypass and circulatory
44: 1501–1509. arrest. Circulation. 1995; 92: 2226–2235.
MCQs
True or False 5. Match the following drugs and their mechanisms of
1. Suspected total anomalous pulmonary venous drainage action in treating pulmonary hypertension:
(TAPVD) in a blue baby is a contraindication for start- (a) Inhaled nitric oxide 1. cAMP pathway mediated
ing prostaglandin E1 or E2 therapy. vasodilation
2. Hyperoxia test reliably distinguishes between congenital (b) Bosantan 2.
Nitric oxide synthase
cyanotic heart disease and PPHN. (NOS) pathway
3. Cardioversion is the treatment of choice for neonatal
atrial flutter. (c) Sildenafil 3.
Phosphodiesterase 5
4. In a neonate following Norwood operation with a modi- inhibitor
fied BT shunt, systemic saturations in the 90s is highly (d) Prostacyclin
4.
Endothelin receptor
desirable. antagonist
(e) Arginine 5.
Phosphodiesterase 3
inhibitor
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Section 7
Chapter
Grown-up Congenital Heart Disease (GUCH)
51 Patients in the Cardiothoracic Intensive

Care Unit
Susanna Price and Niki Walker
Introduction of the general population. In addition, some of the

commonly occurring medical presentations that any
The numbers of patients with congenital heart dis-
intensivist may face will be addressed, together with
ease (CHD) surviving to adulthood are increasing
management of the postoperative GUCH patient.
due to advances in both surgical and interventional
cardiological techniques. In the USA it is estimated
that >10 × 106 adult patients have CHD (grown-up Principles of Management of the GUCH
congenital heart disease, GUCH), and in the UK Patient on the ICU
the number of adult patients with moderate-severe
lesions is predicted to increase by approximately 1600 General Principles
per annum. The commonest indication for reinter- Patients are generally classified as having simple,
vention in GUCH is for treatment of dysrhythmia; moderately complex and complex congenital heart
however, this only rarely directly demands intensive disease according to the Canadian Consensus defini-
care admission. tions, with increasing complexity of disease associ-
Most GUCH patients requiring ongoing medical ated with higher ICU interventions, morbidity and
and critical care attention are at the more severe end of mortality. Approaching such patients when critically
the disease spectrum, requiring repeated interventions ill demands application of a number of basic princi-
to replace valves or conduits, and to address persistent/ ples. The first principle of GUCH ICU management
worsening haemodynamic compromise. Critical care is to understand the cardiopulmonary anatomy of the
of the adult GUCH patient can be extremely chal- individual patient. This involves knowledge of the pri-
lenging, as the pathophysiology of the patient may mary lesion, the type of any corrective/palliative sur-
be complex, and response to usual intensive care gery or intervention performed, and the presence of
interventions unpredictable or even harmful. In such any residual haemodynamic lesions –either dynamic
patients, morbidity and mortality have been shown to or fixed. Second, an understanding of the normal
increase with increasing complexity of disease; there- physiology of the patient is essential. This includes the
fore expert advice should be sought, particularly at the normal haemoglobin, oxygen saturations, systemic
complex end of the spectrum. Although recommenda- and pulmonary blood pressure and surface electro-
tions are that critically ill GUCH patients be managed cardiogram. Third, the ICU clinician must consider
in specialist centres, where they present with medical how the effects of any supportive and therapeutic
emergencies, there may be insufficient time to trans- interventions might affect the circulation. This is of
fer for treatment. Thus all cardiothoracic intensivists particular importance in the univentricular heart, in
should have the knowledge and skills to assess and the presence of systemic-pulmonary shunts and in
manage these patients whilst seeking expert advice. the Fontan circulation. In GUCH patients (particu-
This chapter will outline the general princi- larly where complex) performance of relatively simple
ples involved in the care of the critically ill GUCH investigations and interventions may differ from those
patient, particularly where they differ from those in the non-GUCH population. In addition to the basic
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Table 51.1 General considerations in the critically ill GUCH patient
Pulmonary/respiratory Cardiovascular Renal, GI, endocrine, fluids

Difficult intubation: multiple GUCH Absent or abnormal connections expected, May have associated asplenia, GI or renal
lesions associated with difficult i.e. Fontan or TCPC, or unexpected, i.e. malformations
intubation persistent LSVC
Associated congenital pulmonary Multiple previous arterial/venous Renal impairment is common, particularly
disease: i.e. hypoplastic lung/lung tissue/ cannulations, difficult vascular access – in cyanotic patients, and is associated with
severe congenital V/Q mismatch ultrasound may be essential increased mortality
Lung reperfusion injury: ARDS-like Air filters on all lines in patients with Severe right heart failure may necessitate low
picture (unilateral/bilateral) may occur potential for right-left shunting rates of enteral feeding where cardiac output
is borderline
Difficulty weaning: associated congenital Cardiac output measurement Abnormal liver function is common, and
musculoskeletal deformities • Output from the right and left heart may associated with increased postoperative
differ – shunt mortality post cardiac surgery
• May be no PA, or right sided
connection –PA catheters unusable
• Oesophageal Doppler –calibration
depends upon aortic dimensions
Previous cardiac surgery: possible phrenic Transvenous pacing, may have no access to High incidence of abnormal thyroid function
nerve palsy the heart from the venous circulation (e.g. in GUCH patients –associated with increased
Fontan circulation) ICU mortality
Difficult tracheostomy: presence of ECG, atrial re-entry tachycardia may Tolerance of fluid loading varies depending
collaterals, abnormal neck/trachea mimic sinus tachycardia, comparison with on the underlying diagnosis, i.e. TV repair
previous ECGs essential versus Fontan/TCPC
Pulmonary hypertension: may need Differential effects of vasoactive drugs on Patients with preoperative erythrocytosis
treating, care where possibility to shunt pulmonary and systemic vasculature may may require higher haemoglobin levels
bidirectionally have unpredictable effects on CO and postoperatively than is generally accepted
saturations on the ICU
Abbrevations: TCPC total cavopulmonary connection; LSVC left superior vena cava; GI gastrointestinal; V/Q ventilation/perfusion; ARDS
adult respiratory distress syndrome; PA pulmonary artery; ICU intensive care unit; ECG electrocardiogram; TV tricuspid valve.
anatomy and physiology, there are further aspects recommended, and iron deficiency in these patients
relevant to ICU care that must be considered in this is common. Haemostatic changes including abnor-
patient population (Table 51.1). malities of prothrombin time, partial thromboplastin
In all patients, close liaison between specialists in time, factors V, VII, VIIII, IX and thrombocytopenia
GUCH, heart failure, congenital cardiac surgery and have been documented, but will not usually require
echocardiography is crucial as the management of treatment. When assessing the cyanotic patient, cit-
such patients demands a multidisciplinary approach. rate bottles adjusted for the haematocrit must be used.
Renal dysfunction is common and occurs due
to the combination of hyperviscosity with arteriolar
The Cyanotic Patient vasoconstriction, resulting in renal hypoperfusion
Cyanotic congenital heart disease is not a contrain- and progressive glomerulosclerosis, manifesting as
dication to ICU admission as such patients may have proteinuria, hyperuricaemia or varying degrees of
a relatively good prognosis, with mortality gener- renal failure. Where a cyanotic patient is admitted
ally related to the admission diagnosis. The cyanotic with abnormal neurology, headache or is postictal,
patient has adaptive mechanisms to increase oxygen a high index of suspicion should exist for intracer-
delivery, including a rightward shift in the oxyhae- ebral thrombosis, haemorrhage or abscess. Where
moglobin dissociation curve, an increase in cardiac intravenous contrast is used, the patient must be well
output, and an increased haematocrit. The result- hydrated, and the minimal amount of contrast used as
ant erythrocytosis may result in the hyperviscos- possible, as there is the potential to develop marked
ity syndrome; however routine venesection is not hyperkalaemia following administration.
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Chapter 51: Grown-up Congenital Heart Disease Patients
The Failing Morphological Right Ventricle PVR may result in an increase in systemic-pulmonary
shunting with fall in cardiac output. Attention should
The morphological right ventricle (RV) may be sub-
also be paid to oxygen administration, as this may also
pulmonary, subaortic or be the only effective ventricle
alter the balance between pulmonary and systemic
in the univentricular heart. Causes of right ventricu-
circulation.
lar dysfunction include previous cardiac surgery, pul-
monary hypertension, Ebstein’s anomaly, a significant
shunt, systemic RV and volume overload. The subpul- Medical Indications for ICU Admission
monary failing RV may be supported using standard
inotropic agents whilst avoiding pulmonary vaso-
in the GUCH Patient
Mortality in GUCH patients requiring ICU admis-
constrictors. Cardiac output may be maintained or
sion for medical indications (excluding arrhythmia) is
improved by minimising RV afterload: minimising
high (36%) and accurately predicted by the APACHE
ventilator pressures, drainage of pleural collections,
II score. Where the indication for admission is non-
bronchodilation, the use of pulmonary vasodilators
cardiological, the principles of management of the
and early extubation.
admission diagnosis are the same as for the non-
Where the morphological RV is systemic (con-
GUCH population.
genitally corrected transposition of the great arteries
(ccTGA) and transposition of the great arteries (TGA)
with Mustard/Senning) and failing, treatment is chal- Arrhythmia
lenging. Reversible causes (including arrhythmia and The commonest indication for hospital admission in
volume overload) should be aggressively sought and the GUCH population is arrhythmia, and on occa-
treated. Although systemic RV fibrosis is common, sion this will require ICU admission, or input from
the coronary arteries are usually angiographically the critical care team. The management of arrhythmia
unobstructed. Standard management of the failing in the ACHD ICU population is complex; however
systemic ventricle should be used, including pharma- some general principles should be considered. First,
cological and mechanical support, but these may not the diagnosis of an arrhythmia may be challenging;
be effective. In some centres the use of multisite RV atrial tachycardia may mimic sinus tachycardia to the
pacing has been used with good effect. non-expert. Here, comparison with previous 12-lead
ECGs is useful, and where a pacemaker is implanted,
The Univentricular Heart interrogation may be critical in making the diagno-
sis. Second, as there is a high incidence of thyroid
This presents many challenges, from prevention of air
dysfunction and amiodarone prescription in the
embolism, to the unpredictability of the effects of vas-
GUCH population, thyroid function tests should be
oactive agents and the adverse effects of positive pres-
performed upon diagnosis of a tachycardia or brady-
sure ventilation. It is important to know the current
cardia. Third, although patients with a univentricular
and most previously documented function of the sin-
circulation in atrial tachycardia may tolerate a tach-
gle ventricle (morphologically right or left), as recent
yarrhythmia well initially, decompensation may be
rapid deterioration is often due to development of an
rapid, and cardioversion should be considered at the
arrhythmia. Expert echocardiography is indicated.
earliest opportunity. Such patients should be man-
When considering the use of inotropic and vasoactive
aged by the most senior clinician, as cardioversion to a
agents, the nature of the pulmonary connections must
malignant arrhythmia is not uncommon, and as there
be considered. Where the pulmonary vasculature is
may be no venous access to the heart. Transcutaneous
protected by PA banding, the relative effects of pulmo-
pacing must always be available.
nary versus systemic constriction or dilatation may be
different when compared with where there is an absent
pulmonary connection with systemic- pulmonary Heart Failure
collaterals/shunts. In the patient with absent pulmo- The causes of heart failure in the GUCH population
nary connection and systemic-pulmonary collaterals/ include one or more of: impaired ventricular function
shunts a small increase in PVR may result in a signifi- (left or right), volume overload, arrhythmia, valve
cant reduction in pulmonary blood flow and desatu- lesions or an excessive shunt. Once an arrhythmia has
ration. In contrast, an increase in SVR and/or a fall in been excluded, echocardiography is required to make
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or confirm the diagnosis. Where indicated, urgent unlike in medical GUCH admissions, standard scor-
surgical or catheter intervention may be required. ing systems do not reflect the severity of illness of
Pre-optimisation of cardiac output prior to surgery the patients as they tend to overestimate mortality in
has not been shown to improve patient survival, but those with more simple disease, and underestimate
if possible pulmonary oedema and sepsis should be predicted mortality in those with more complex dis-
treated prior to any run on bypass. Once surgically ease. In specialist centres perioperative mortality
or catheter-directed correctable causes have been and morbidity is low, but increases significantly with
excluded, management is directed to treating ventric- increasing disease complexity, and in the presence of
ular dysfunction. preoperative abnormalities in renal, liver or thyroid
function. As in the paediatric population, haemody-
Haemoptysis namically significant residual lesions postoperatively
are associated with a significantly increased ICU mor-
Haemoptysis in this population –particularly those
bidity. Good postoperative management relies on a
with pulmonary hypertension –should always be con-
clear understanding of not only the underlying dis-
sidered a serious event, and early transfer to high level
ease, but also the precise surgical procedure and out-
care with advanced airway skills immediately available
come, and also the haemodynamic responses of the
is important. Minor haemoptysis may herald a major
patient in the operating theatre. Close liaison with and
bleed, and patients with major haemoptysis usually
detailed handover from the operating surgeon and
die due to their unprotected airway rather than blood
cardiac anaesthetist are essential.
loss. Haemoptysis in the GUCH population has been
attributed to bronchitis, bleeding diathesis, pulmonary
arterial rupture, pulmonary embolism, tracheoarte- Simple Congenital Heart Disease
rial fistula (in prolonged intubation or tracheostomy)
and rupture of aortopulmonary collaterals. In patients Atrial Septal Defect (ASD)
with Eisenmenger physiology, haemoptysis accounts The treatment of choice for closure of ASDs is percu-
for 11–15% of deaths. Investigation will depend upon taneous device closure; however, some large or com-
the skills available locally, but would normally include plex defects will require surgical closure. Although
plain chest radiography, CT angiography and angiog- in the younger patient population the procedure is
raphy, with a view to embolisation, where it may be well tolerated, there is a high incidence of postopera-
life saving. tive arrhythmia. Pulmonary hypertension recorded
preoperatively may not resolve immediately, but in
Endocarditis the presence of an adequate cardiac output may not
require treatment. The more elderly patient may have
The diagnosis of endocarditis requires physicians to
restrictive ventricular disease, which limits cardiac
have a high index of suspicion, the performance of
output. Where diagnosed, pacing should be optimised
multiple blood cultures, and expert echocardiography.
using echocardiography and continuous cardiac out-
Echocardiography to exclude evidence of infection in
put monitoring (usually avoiding right heart cath-
this patient population is particularly challenging as
eterisation) to optimise the cardiac output and may
it may not be confined to intracardiac structures. On
require heart rates of up to 130 beats per minute.
occasion nuclear medicine (PET CT) and/or cardiac
magnetic resonance scanning may give further indica-
tion as to the site of infection. Multidisciplinary team Moderately Complex Congenital Heart
working, including the endocarditis team, is essential Disease
at an early stage following diagnosis.
Atrioventricular Septal Defect (AVSD)
Surgical/Postoperative Admissions Complete AVSD repair is usually performed in child-
hood; however, some adults may present with par-
in GUCH tial defects requiring surgical repair. Here the most
The majority of GUCH patients requiring ICU admis- important determinant of outcome is a successful
sion will be postoperative. Here the mortality relates surgical repair –in particular ensuring the absence of
to the complexity of the underlying disease; however, left ventricular outflow tract obstruction (LVOTO).
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Where a patient has inadequate cardiac output post- such cases, the added burden of significant volume
operatively, in addition to exclusion of the usual post- overload on the systemic morphologically RV may
operative complications, LVOTO should specifically result in significant ventricular dysfunction postop-
be excluded using echocardiography. eratively (The Failing Morphological Right Ventricle).
Where required in the postoperative period, mechani-
Tetralogy of Fallot (TOF) cal circulatory support may be considered whilst the
Patients admitted postoperatively with a diagno- RV recovers from the surgical insult. Where associ-
sis of TOF will either have undergone redo-surgery ated with a small left (subpulmonary) ventricle, either
(usually pulmonary valve replacement) or, less fre- with or without a LV-PA conduit, care must be taken
quently, primary repair. Although primary repair in to avoid left LVOTO as a result of inotropic sup-
the adult population is associated with significant port required for the RV. Here, aortic balloon coun-
ICU morbidity, even redo-surgery for pulmonary terpulsation may be useful by providing systemic
valve replacement should not be regarded as ‘rou- RV support and minimising the need for inotropic
tine’. Complications and morbidity are usually asso- administration.
ciated with right ventricular dysfunction. However,
significant left ventricular dysfunction may coex- Transposition of the Great Arteries (TGA)
ist, particularly in the presence of coronary artery Patients admitted to the ICU following surgery for
disease. In patients undergoing primary repair the TGA will have undergone either a Rastelli procedure
increased pulmonary blood flow may result in pul- (physiologically normal communications), Mustard/
monary capillary hyperpermeability, presenting with Senning (systemic RV, subpulmonary LV) or arterial
an ARDS-like picture, and managed as is standard switch (normal connections). The postoperative man-
for acute lung injury post-bypass. agement of these patients illustrates the importance of
understanding the underlying anatomy, surgery and
Ebstein’s Anomaly physiology of the ACHD patient.
The postoperative course of these patients is deter- In a Rastelli procedure, the normal ventriculoar-
mined by the amount and function of the postop- terial connections are restored, and adult patients are
erative RV, meticulous intraoperative management generally admitted following redo-surgery for con-
(surgical and anaesthetic), and the technical expertise duit replacement. In patients with previous Mustard/
of the surgeon. Where there is significant RV dysfunc- Senning procedures the systemic ventricle remains
tion, this should be managed in the standard way. morphologically a RV –thus postoperatively these
Significant postoperative RV dysfunction is associated patients have a higher incidence of ventricular dys-
with a high incidence of renal, gastrointestinal and function and have a greater requirement for car-
hepatic dysfunction, and a significant requirement for diorespiratory support. Where patients undergo
prolonged respiratory support. If the cardiac output surgery for systemic baffle revision for baffle obstruc-
is inadequate despite all measures and an intra-atrial tion, chronic venous hypertension results in hepatic
communication does not exist, atrial fenestration and renal dysfunction, which does not resolve imme-
may be considered in the absence of significant left diately, and is associated with significant postopera-
ventricular disease. The postoperative Ebstein’s tive morbidity in some cases. In an arterial switch
patient has a high incidence of atrial arrhythmias and procedure, the ventriculoarterial connections are
these should be managed in collaboration with an anatomically normal; however, late complications in
electrophysiologist. adulthood include requirement for aortic or pulmo-
nary valve replacement, and ventricular dysfunction
due to coronary disruption. In these patient popula-
Complex Congenital Heart Disease tions, postoperative recovery is generally uneventful,
and does not significantly differ from standard post-
Congenitally Corrected Transposition of the Great cardiac surgical care.
Arteries (ccTGA)
Surgery in this patient population usually relates to Systemic-Pulmonary Shunt
requirement for tricuspid valve replacement (the sys- Patients with either central or Blalock–Taussig type
temic atrioventricular valve) due to regurgitation. In aortopulmonary shunts rely on systemic arterial
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pressure to maintain pulmonary blood flow via the and is intubated, ventilator settings and fluid balance
shunt. In such patients, pulmonary blood flow may be may be titrated against venous return using echocar-
reduced by aggressive ventilatory manoeuvres but the diography. In patients with a fenestrated circulation,
major determinant of pulmonary blood flow remains the presence of hypoxia may represent V/Q mismatch
systemic aortic pressure, and therefore desaturation or excessive right-left shunting through the fenestra-
may require the use of systemic vasoconstriction. tion. Differentiating between the two is important,
GUCH patients previously palliated with either as hypoxia resulting in pulmonary vasoconstriction
classical or modified Blalock– Taussig shunts will will limit cardiac output. Here, echocardiography may
exhibit reduced arterial pressure in the ipsilateral arm, also be useful.
ranging from slight under-reading compared to aortic The postoperative recovery of these patients is
pressure to almost impalpable arm pulses. unpredictable, ranging from immediate extubation
and ICU discharge to prolonged ICU admission with
Fontan and Fontan-Type Circulations multisystem dysfunction, a high incidence of coagu-
Surgery undertaken in this patient population is usu- lopathy, renal dysfunction, hepatic dysfunction and
ally elective, comprising conversion from atriopul- requirement for ventilatory support, particularly
monary Fontan to total cavopulmonary circulation where surgery is undertaken in the presence of a sig-
(TCPC). The physiological effects of a univentricu- nificantly obstructed Fontan circulation associated
lar circulation together with systemic venous hyper- with a very low cardiac output state.
tension over years in these adult patients present
challenges to the intensivist in their postoperative
management. Having a prolonged univentricular cir-
Conclusion
culation results in ventricular dysfunction that should Management of the critically ill GUCH patient requires
be managed using standard supportive measures (ino- a highly trained multidisciplinary team approach, and
dilators, pacing, mechanical support). Arrhythmias although it is best carried out in specialist centres, with
are common, and may be difficult to diagnose, particu- improving patient survival patients will inevitably
larly when temporary epicardial pacing is undertaken increasingly present to their local hospitals. Although
postoperatively. Where there is any haemodynamic training all intensivists in this interesting and complex
disturbance an ECG (including atrial leads) should be specialty is not realistic, knowledge of the basic prin-
performed. Prevention of atrial arrhythmias is impor- ciples of assessment and management of the critically
tant, as they will significantly reduce cardiac output ill GUCH patient is important. Early discussion with
in these patients, with close attention to electrolytes, the specialist centre is vital.
early administration of amiodarone and cardioversion
where indicated. Learning Points
The passive flow of blood from the systemic • Investigation and management of the
venous circulation to the pulmonary circulation critically ill GUCH patient is complex and
depends upon adequate preload and avoidance of pul- requires input from an appropriately trained
monary hypertension. When the patient is mechani- multidisciplinary team.
cally ventilated, positive pressure significantly reduces
• The key to good management involves
cardiac output. Thus, in order to maximise cardiac
understanding the cardiopulmonary anatomy and
output, pulmonary vascular resistance and intratho-
physiology of each individual patient.
racic pressure should be kept as low as possible, with
• Standard ICU parameters in the non-GUCH
aggressive drainage of pleural collections, avoidance
population may not be applicable in the GUCH
of pulmonary vasoconstrictors, treatment of bron-
patient.
choconstriction, pulmonary vasodilators, minimising
ventilator pressure settings and extubation as early as • The response to standard ICU therapies may be
the patient allows. Respiratory failure will, however, unpredictable.
also adversely affect this patient population, and the
benefits of early extubation need to be carefully bal- Further Reading
anced against the requirement for ventilatory sup- British Cardiac Society Working Party. Grown-up
port. Where the patient needs respiratory support congenital heart (GUCH) disease: current needs
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and provision of service for adolescents and adults randomized clinical trial. Journal of Vascular Surgery.
with congenital heart disease in the UK. Heart. 2002; 2002; 35: 631–639.
88(Suppl 1): i1-i14. Daliento L, Somerville J, Presbitero P, et al. Eisenmenger
Cheung AT, Pochettino A, Mc Garvey ML, et al. Strategies syndrome. Factors relating to deterioration and death.
to manage paraplegia risk after endovascular stent European Heart Journal. 1998; 19: 1845–1855.
repair of descending thoracic aortic aneurysms. Annals O’Sullivan JJ, Wren C. Survival with congenital heart
of Thoracic Surgery. 2005; 80: 1280–1288. disease and need for follow-up into adult life. Heart.
Child JS, Collins-Nakai RL, Alpert JS, et al. Bethesda 2001; 85: 438–443.
Conference Report –Task Force 3: Workforce Price S, Jaggar SI, Jordan S, et al. Adult congenital heart
description and education requirements for the disease: intensive care management and outcome
care of adults with congenital heart disease. prediction. Intensive Care Medicine. 2007; 33: 652–659.
Journal of the American College of Cardiology. 2001;
37: 1183–1187. Warnes CA, Liberthson R, Danielson GK, et al. Bethesda
Conference Report –Task Force 1: The changing
Coselli JS, Le Maine SA, Köksoy C, et al. Cerebrospinal profile of congenital heart disease in adult life.
fluid drainage reduces paraplegia after Journal of the American College of Cardiology. 2001;
thoracoabdominal aortic aneurysm repair: results of a 37: 1170–1175.
MCQs
1. In a GUCH patient with a significant shunt, which of 4. In a patient with univentricular circulation, what is
the following are reliable indicators of cardiac output? the potential effect of giving an inodilator? (more than
(more than one answer may be correct) one answer may be true)
(a) Oesophageal Doppler (a) Increase in pulmonary circulation due to reduced
(b) Pulmonary artery catheter pulmonary vascular resistance
(c) PiCCO (b) Increase in cardiac output due to reduced systemic

vascular resistance
(d) LiDCO
(c) Increase in saturations associated with an increase
(e) Thoracic impedance in systemic blood flow
2. Adaptive mechanisms in the cyanotic patient include: (d) Fall in saturations associated with an increase in
(a) A leftward shift in the oxyhaemoglobin systemic blood flow
dissociation curve (e) Increase in saturations associated with a fall in sys-
(b) A fall in cardiac output temic blood flow
(c) Polycythaemia 5. A GUCH patient is admitted to the ICU following a
laparotomy. You are told they have had a repair for
(d) Erythrocytosis
Tetralogy of Fallot. Which of the following statements
3. In a patient with arrhythmia, which of the follow- are true? (more than one answer may be true)
ing require cardioversion as soon as possible, even
(a) A previous Blalock–Taussig shunt will mean ipsilat-
if haemodynamically stable? (more than one answer
eral blood pressure monitoring may be inaccurate
may be correct)
(b) The potential for intracardiac shunting still exists
(a) Congenitally corrected transposition of the great
arteries (c) The morphological right ventricle is systemic
(b) Transposition with an arterial switch (d) The patient is expected to be erythrocytotic
(c) Severe pulmonary regurgitation (e) Echocardiography is indicated, even if
haemodynamically stable
(d) Fontan circulation
(e) Ebstein’s anomaly
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Section 7
Chapter
Difficult to Wean from Mechanical
52 Ventilation Patients in the Cardiothoracic

Intensive Care Unit
Michael G Davies
Introduction the patient can breathe spontaneously and protect the

airway. A two-step process is used to ensure that extu-
Weaning from invasive mechanical ventilation (IMV)
bation may be considered. Firstly, safe clinical param-
may be classified as simple, difficult or prolonged. Each
eters need to be achieved (screening) followed by a
category presents its own distinct clinical manage-
weaning trial (spontaneous breathing trial).
ment issue. More than 75% of patients achieve simple
weaning, namely extubation at first attempt. For such
patients, the aim is to identify the soonest opportunity Screening Parameters for Early Extubation
to resume spontaneous breathing. Shorter durations Clinical criteria for early extubation following elec-
of IMV can reduce morbidity and the duration of ICU tive, uncomplicated cardiac surgery include:
admission, therefore providing benefit at both individ- • haemodynamic stability (satisfactory rhythm,
ual and institutional level. Difficult weaning is defined blood pressure and urine output),
as requiring up to three spontaneous breathing trials • adequate rewarming, haemostasis and metabolic
or up to 7 days. Finding the cause of failed extubation status,
is of paramount importance, since these patients are • intact neurological function,
at a clinical threshold; some will proceed to a recovery • satisfactory respiratory and upper airway
that is free from further complication, whereas others function.
will succumb to other complications and may deterio-
rate towards multiorgan failure. Finally, patients who
experience prolonged weaning (more than 7 days) Using Protocols to Achieve Earlier
form a small minority, but are an important clinical Extubation
problem. Despite surviving the acute problem(s), they For low-risk patients returning to critical care after
remain in respiratory failure and continue to require elective surgery, a significant part of clinical decision-
IMV for prolonged periods. This has a disproportion- making relates to the timing of extubation. We know
ate effect upon ICU bed occupancy due to long ICU from studies of unplanned extubations that a size-
admissions. The distinct multidisciplinary expertise able proportion of patients who self-extubate do not
required to make progress in this patient group may require reintubation. This indicates that the opportu-
not be available in a standard cardiothoracic critical nity for earlier extubation for some patients may have
care unit. This chapter will review the clinical chal- been missed by the clinicians. Formal weaning proto-
lenges provided by each weaning category, although it cols have emerged to reduce the delays in the pathway
will focus upon the management of patients who have towards extubation. Following cardiac surgery, such
required prolonged IMV. strategies are associated with a reduced ICU length of
stay and no increase in morbidity if compared to non-
Simple Weaning fast-track care. Protocols and even automated weaning
Following uncomplicated and successful surgery, rapid may therefore improve the organisational efficiency of
weaning is expected. Ideally, IMV should be stopped a critical care unit with a high throughput of elective
as soon as the reason for ventilation has resolved and surgery. These strategies are often packaged together
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Chapter 52: Difficult to Wean from Mechanical Ventilation
with other aspects of care, focused on achieving early the transition from supported to unsupported breath-
discharge from critical care for patients judged to be at ing may cause haemodynamic decompensation.
low risk preoperatively. Reducing ICU length of stay It is just as important to note that extubation delay
by a small amount for a large number of patients may identifies the individual patient as at high risk of new
reduce ICU bed occupancy, resulting in increased complications; in the presence of extubation delay, a
opportunity for surgical activity. cascade of additional problems are more likely, includ-
ing multiple-organ failure and death.
Difficult Weaning
Difficult weaning is defined as failing a weaning trial Role of Checklists and Prompts
and requiring up to three trials of spontaneous breath- Extubation is an important part of the process towards
ing or a period of up to 7 days to achieve extubation. recovery of function and discharge from the ICU.
For patients in cardiothoracic critical care, this cohort Failure to extubate may delay other processes such as
may be identified as those who experience ‘extubation intravascular line and urinary catheter removal. With
delay’. increasing duration of IMV, there are increased rates of
nosocomial infections. Alongside efforts to optimise
Extubation Delay cardiorespiratory function in preparation for extuba-
A sequential audit of unselected adult cardiac surgery tion, general clinical stability needs to be maintained.
patients found that extubation was achieved within 6 The development of an infection or other complica-
hours of surgery for 39% of patients, within 24 hours tion at this key time point can lead to a spiral of clini-
for 89% and within 48 hours for 95%. An extubation cal deterioration leading to death or prolonged IMV.
delay >48 hours after CABG is associated with longer Strategies to reduce ICU associated complica-
ICU and hospital stays, and increased mortality. tions have been shown to improve patient outcomes.
Factors associated with extubation delay are summa- Given the complexity of critical care medicine, human
rised in Table 52.1. errors of omission in decision-making are especially
As shown, patients who experience extubation important and can further delay weaning from IMV.
delay are characterised by preoperative comorbidity The introduction of checklists and prompting are
and/or adverse perioperative and postoperative events. synonymous with attempts to reduce human error.
Whilst respiratory factors, such as COPD, may have Checklists reduce the incidence of catheter- based
a role, for many patients the rate-limiting problem is bloodstream infection and urinary sepsis and, when
cardiac in nature. The spontaneous breathing trial is, combined with active prompts, ICU length of stay and
in effect, a type of exercise and will increase cardiac mortality are reduced. In one study the most signifi-
output requirements. If cardiac reserve is limited, then cant effect was seen for patients in the third quartile of
predicted risk (i.e. neither low risk or at highest risk of
death). For such ‘medium-risk’ patients, hospital mor-
Table 52.1 Factors associated with extubation delay in
cardiothoracic critical care tality was 8% if active prompting was used, compared
to 33% for those who received usual care. Of course,
Variable preventing nosocomial infection is important for all
Preoperative ↑ Renal dysfunction patients; however, these data suggest that medium-
↑ NYHA stage risk patients, as evidenced by extubation delay, repre-
COPD (reduced FEV1) sent a clinical threshold in which infection avoidance
Emergency surgery usually leads to rapid discharge from ICU, whereas
Female gender
the development of infection confers a more challeng-
ing prognosis.
↑ Age
Operative ↑ Perfusion time
↑ Blood loss
Role of Non-invasive Ventilation (NIV)
Non-invasive ventilation (NIV) refers to the delivery
Postoperative ↑ Blood loss
of ventilatory support using a mask, rather than an
↑ Inotrope requirement
endotracheal or tracheostomy tube. Increasing recog-
Arrhythmia
nition of its role in preventing the need for intubation
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in deteriorating patients has led to its use following ‘chronic critical illness’ has emerged, namely patients
extubation in selected patients. NIV may be delivered who continue to require life-sustaining organ support
prophylactically after extubation if the patient is con- following acute critical illness. Prolonged dependence
sidered to be at high risk of respiratory failure, or as on IMV, a key feature of chronic critical illness, has
rescue therapy in the event of unanticipated postextu- emerged as a significant public health challenge, with
bation respiratory failure. annual costs in the USA estimated to be $35 billion.
A Cochrane systematic review showed that NIV Patients who experience prolonged IMV have
reduced the rate of reintubation and ICU length of higher mortality and occupy a disproportionate num-
stay for selected patients. Identifying suitable patients ber of ICU bed days, leading to increased health care
for NIV requires an understanding of its physiologi- costs. However, after IMV has continued for 15 days
cal action. NIV acts as an additional respiratory pump or more, fewer patients have multiple-organ failure
to improve alveolar ventilation and, as such, reduce and mortality rates start to plateau. Most surviving
hypercapnia. Patients most likely to benefit from NIV patients enter a state of limbo, achieving relative clini-
are those who demonstrate evidence of, or a predis- cal stability but continuing to require ICU support for
position towards, hypercapnia. Patients at risk include single-organ respiratory failure. Protocols or auto-
those with a pre-existing problem with their respira- mated changes in ventilator settings, used with success
tory muscle pump, such as COPD or neuromuscular in simple weaning, have little impact upon the patients
conditions, and those who develop a degree of hyper- who lack the capacity to breathe independently.
capnia during a spontaneous breathing trial. Trial data
support this assertion, showing that NIV provides sig- Role of the Specialised Weaning Unit
nificantly greater mortality benefit in trials enrolling
An international consensus document concluded that
patients with COPD compared to trials that included
standard critical care units may lack the necessary
mixed patient populations.
focus and structure to manage patients with weaning
Whilst the use of NIV to permit earlier extuba-
failure. On any given day, competing demands for the
tion and prevent reintubation is likely to evolve fur-
critical care team include new admissions and exist-
ther, current data support its use for selected patients.
ing patients with acute instability or complex multiple
The success of NIV is also reliant upon the expertise
organ failure. In such circumstances, it may be easy to
of the team who are delivering it. In some healthcare
maintain the clinical stability of the patient with wean-
systems, such as the UK, NIV has evolved as a ward-
ing failure, but more challenging to make progress.
based practice. If competence in applying NIV and
A variety of organisational models have emerged.
troubleshooting are lacking, then treatment failure is
Long- term acute care hospitals (LTACHs) manage
more likely.
patients with persisting failure of a range of organ sys-
tems, including weaning from IMV, whereas special-
Prolonged IMV (Weaning Failure) ised weaning units focus on weaning from IMV alone.
The NHS Modernisation Agency Weaning and Long Both service models use lower staff to patient ratios
Term Ventilation Group defined weaning failure as than critical care units and therefore offer an eco-
the need for IMV for 3 weeks or more, at least three nomic advantage. The recommended model of care in
previous failed weaning trials, and in the absence of the UK is the specialised weaning unit.
any non-respiratory cause.
Factors Associated with Weaning Failure
Impact of Prolonged IMV Successful respiration depends upon an adequate
Approximately 5– 10% of ICU patients experience capacity to breathe (respiratory capacity). Respiratory
prolonged weaning failure and continue to require capacity requires an adequate muscle pump that
IMV for periods exceeding 3 weeks. Numerous fac- receives appropriate signals from an intact neuro-
tors contribute to prolonged IMV; advances in critical logical system. The control of respiration (respira-
care have led to an increasing proportion of patients tory drive) is complex and regulated by a number of
who survive the acute episode and also to an older physiological mechanisms, some via the automatic
and increasingly frail patient population accessing system (e.g. chemoreceptors sensitive to hypercapnia
complex surgery and critical care. The concept of and hypoxia) and some via voluntary control during
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wakefulness. In simple terms, weaning failure reflects

an imbalance between the respiratory capacity and
Approach to the Patient with Weaning
the opposing force of workload applied (respiratory Failure
load). Impaired respiratory drive is uncommon in this There are limited data regarding the recommended
patient population, assuming that excessively high management approach for patients who have expe-
PaCO2 levels are avoided. rienced weaning failure. However, features that are
When assessing the reasons for weaning failure, it common to published series from specialised weaning
is helpful to consider the relative impact of opposing units include the following.
forces of capacity and load. Identifying such factors
leads to a clearer management plan, both with respect Ventilate to Normalise Gas Exchange before Weaning
to weaning in the short term and also in considering Liberation from IMV is more likely to succeed if
the level of long-term respiratory support that may gas exchange is stable and satisfactory. Despite this,
be needed. Common factors associated with weaning patients admitted to specialised weaning units typi-
failure are summarised in Table 52.2. cally demonstrate hypercapnia and an elevated plasma
bicarbonate concentration. Several factors may con-
tribute, including relative underventilation, electro-
Table 52.2 Common factors associated with weaning failure lyte disturbance (hypochloraemia, hypokalaemia and
hypophosphataemia), hypoalbuminaemia, and the
Decreased respiratory capacity
prior use of diuretics and steroids. Chronic hyper-
Neurological Cerebrovascular capnia blunts the respiratory drive, whereas reduc-
Critical illness neuropathy ing PaCO2 and bicarbonate concentrations towards
Guillain–Barré syndrome the normal range leads to an improved minute ven-
Myaesthenia tilation response to PaCO2. A decreased response to
Comorbid condition (e.g. motor CO2, as measured by hypercapnic drive and ventila-
neurone disease) tory response, is associated prolonged failure to wean
Muscle weakness Deconditioning from IMV.
Critical illness myopathy Hence, ventilation should be optimised and
Nutritional imbalance increased if necessary. Reducing PaCO2 causes a tem-
Electrolyte imbalance
porary respiratory alkalosis until renal compensation
of bicarbonate occurs. Weaning should not com-
Comorbid condition (e.g.
muscular dystrophy)
mence until this acid-base imbalance has resolved.
Clinical stability needs to be achieved via the ventila-
Increased respiratory load
tor, including satisfactory oxygenation (FiO2 <40%).
Airway related Inadequate tracheostomy
(position, size)
Review the Diagnosis and Factors Associated with
Excessive secretions
Weaning Failure
Bronchospasm
Identifying and minimising any factors contributing
Reduced lung compliance Pneumonia
to weaning failure are vital if weaning is to be achieved.
Parenchymal problems (e.g. Transfer to a weaning unit provides a good opportu-
fibrosis)
nity for diagnostic review, but continual assessment of
Bronchospasm
progress is essential regardless of the location of care.
Obesity An ‘airway, breathing, and circulation’ approach may
Decreased cardiac reserve Reduced LVEF identify new, important clinical issues. For example,
Arrhythmia bronchoscopic evaluation may find excessive secre-
Pericardial collection tions or a poorly located tracheostomy tube. Tracheal
Decreased respiratory drive stenosis is uncommon, but may be the main cause of
Neurological weaning failure for up to 5% of patients. The under-
lying respiratory pathology should also be carefully
Metabolic
considered and there should be a low threshold for
Drug related
thoracic CT. Retrospective series have shown that
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CT scanning impacts management in up to 30% of team. Initial trails of breathing require 1:1 input from
patients with weaning failure. a member of the team who is skilled in weaning from
Weaning is rarely achieved in the setting of per- prolonged IMV. Weaning consists of daytime periods
sistent infection and hypoalbuminaemia. Subacute of unsupported spontaneous breathing, a weaning
infections (respiratory or non- respiratory), usually method that has been shown to be associated with
characterised by a moderate elevation of inflamma- shorter weaning times in this patient group, when
tory markers, should be actively pursued and treated compared to weaning via pressure support. When
aggressively. Pleural effusions are common and possible, the tracheostomy cuff is deflated and a speak-
can be identified, analysed and drained via bedside ing valve employed to encourage communication.
ultrasound. Cardiac status should be reviewed, since Short initial periods of unsupported breathing, usu-
disturbances in cardiac perfusion, rhythm or ventric- ally undertaken in the morning, can build confidence
ular function may affect cardiorespiratory capacity to in the process. Daytime weaning can then progress
wean. Simple non-invasive assessments, such as ECGs according to the respiratory capacity of the patient.
at the beginning and end of a weaning period and Clinical and objective measures of respiratory func-
routine transthoracic echocardiography, can iden- tion should be monitored during the weaning period
tify abnormalities that are contributing to a failure to (e.g. continuous transcutaneous carbon dioxide anal-
wean. In rare circumstances, an additional systemic ysis with blood gas measurement as necessary). On
pathology may be found, such as hypothyroidism or completion of a weaning trial, the patient should be
an inflammatory disease. congratulated and IMV recommenced. Here, the ven-
tilator is not an additional method of weaning, rather
Normalise the Environment it should provide adequate support of breathing (e.g.
Critical care unit design focuses on the ability to mon- pressure control ventilation) to rest and prepare for
itor patients closely and respond quickly in the event the next period of weaning.
of acute problems. However, from a patient’s perspec-
tive some of these measures may be perceived as hos- Use a Multidisciplinary Team Approach
tile and stressful, for example excessive noise arising The multidisciplinary team (MDT) plays a key role in
from early warning alarms (such as ventilator discon- the management of the patient with weaning failure.
nection). Critically ill patients sleep poorly and this is Progress is usually made on a gradual basis and the
due, at least in part, to the critical care environment nursing team is best equipped to provide continu-
itself. ous, holistic assessment. A positive approach towards
Simple interventions such as ear plugs and eye- rehabilitation is required and is achieved by the input
masks may improve subjective measures of sleep of a physiotherapist with expertise in the manage-
quality following cardiac surgery. Whilst data are ment of such patients. Nutritional management can
limited in this area, it is logical that efforts to reduce be complex and benefits from specialist dietetic and
excessive noise, sleep disruption, pain and social isola- speech therapy input. Within our unit, we hold weekly
tion should have a positive impact upon the recovery MDT meetings, attended by all senior members of the
of function. In the same way, positive strategies that medical, nursing, physiotherapy and dietetic teams.
restore normality to circadian patterns of sleeping and Clinical progress is reviewed in detail and a forward
eating (if safe) should be encouraged. Compared to plan is agreed.
the critical care environment, the patient in the spe-
cialised weaning unit may experience fewer adverse Use NIV as Part of the Weaning Process
alarms and disruption. To address this, some criti- Decannulation of the tracheostomy can only be con-
cal care units place less critically ill patients in a less sidered when IMV is no longer necessary. For some
‘intensive’ environment. patients, there is a continued need for ventilatory
assistance at least on a temporary basis overnight.
Wean via Trials of Unsupported Breathing For example, a patient with pre-existing COPD who
Once gas exchange on the ventilator is optimised develops critical illness myoneuropathy following car-
and there is sufficient clinical stability, then weaning diac surgery may now lack the respiratory capacity
should commence. The patient needs to be able to par- for 24-hour independence from the ventilator. NIV
ticipate in the process and requires confidence in the can be helpful as part of the weaning process to build
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up periods of the day in which IMV is not required. only 22% of patients at meta-analysis. Whilst patient
In addition, applying NIV overnight can reduce the selection may explain this disparity in part, sig-
necessity to revert to IMV. Use of NIV in such circum- nificant differences in the organisation of care and
stances requires a tracheostomy tube to be capped use of long-term NIV appear to be more relevant.
off and deflated. The tube should be small enough to Current data support a specialised approach for this
permit airflow around it; if a voice is not achieved via patient group.
use of a speaking valve during the day, then it is less
likely that NIV via mask will provide benefit over- Conclusions
night. In downsizing a tracheostomy, one must also Weaning from IMV is an area of care in which a ‘one
keep in mind that a small change in tube diameter can size fits all’ approach cannot succeed. For patients in
cause a significant increase in the work of breathing if a ‘simple weaning’ category, extubation will proceed
all breathing passes only through the tube. The aim is without difficulty. The challenge for care is to achieve
to provide a safe and successful transition to decan- this as quickly and safely as possible. Protocols that
nulation and any change in airway management must permit earlier extubation by the bedside nurse are
reflect this. favoured. Small improvements in weaning time can
improve unit efficiency, especially for ICUs with a
Weaning to the Most Appropriate Level of Long-Term high elective surgical activity, providing that earlier
Respiratory Support discharge from critical care is achieved. Patients who
Patients who experience weaning failure represent a experience extubation delay and difficult weaning are
self-selecting group of survivors who have not yielded an ‘at risk’ group. Medical input is required to iden-
to the acute episode or its complications, yet remain tify the cause of failure alongside high levels of gen-
in single-organ respiratory failure. Weaning success eral vigilance to avoid new complications. Protocols
in this situation is defined as liberation from IMV and prompts designed to reduce the impact of errors
to either self-ventilation or nocturnal NIV. This rec- of omission have been shown to improve outcomes.
ognises that long-term survival following prolonged Prolonged weaning is an important clinical chal-
IMV is enhanced if long-term NIV is used when it is lenge. Whilst fewer than 10% of patients experience
indicated. In the UK at least, the specialised weaning weaning failure, critical care costs are high due to
service is typically based within a regional long-term bed occupancy rates. Successful long-term survival
ventilation unit that has particular expertise in the use can be achieved via transfer to a specialised weaning
of NIV. unit. Such units provide the distinct expertise that is
required to maximise rates of discharge home and
long-term survival.
Data from Clinical Studies
Numerous clinical studies have reported outcomes
across a range of organisational approaches. A recent Learning Points
meta-analysis has compared outcomes for reported • Strategies to reduce ICU associated
studies of patients who have required prolonged IMV. complications, such as applying checklists aimed
It has provided clear insights into which patients at reducing infection, improve ICU outcomes.
benefit from continued attempts to wean follow- This is especially evident for patients who have
ing prolonged IMV and the optimal organisational experienced extubation delay.
approach to deliver care, although further research • Use of non-invasive ventilation (NIV) may
is needed. The meta-analysis found somewhat sober- facilitate earlier extubation for patients who have,
ing results, with fewer than 50% of patients alive at or are predisposed to, hypercapnia (e.g. patients
1year. However, important differences according to with coexistent COPD).
the organisational approach were found; UK studies • Uncontrolled hypercapnia should be avoided
(regional weaning units) reported significantly better for patients who have experienced prolonged
outcomes than achieved for US studies from post- invasive ventilation. Attempts should be made to
acute care facilities. For example, 75% of patients normalise gas exchange prior to weaning.
transferred to a UK specialised weaning service • A significant proportion of patients who
achieved discharge to their own home, compared to experience prolonged weaning failure will
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continue to require nocturnal NIV following Davies MG, Quinnell TG, Oscroft NS, et al. Hospital
decannulation. outcomes and long-term survival after referral to a
• Due to the specialised nature of care, transfer specialized weaning unit. British Journal of Anaesthesia.
2017; 118: 563–569.
to a dedicated weaning unit is associated
with improved patient survival and discharge Kahn JM, Le T, Angus DC, et al. The epidemiology of
chronic critical illness in the United States. Critical
home rates.
Care Medicine. 2015; 43: 282–287.
Naughton C, Reilly N, Powroznyk A, et al. Factors
Further Reading determining the duration of tracheal intubation in
Blackwood B, Burns KE, Cardwell CR, O’Halloran P. cardiac surgery: a single-centre sequential patient audit.
Protocolized versus non-protocolized weaning for European Journal of Anaesthesiology. 2003; 20: 225–233.
reducing the duration of mechanical ventilation in Pilcher DV, Bailey MJ, Treacher DF, et al. Outcomes,
critically ill adult patients. Cochrane Database of cost and long term survival of patients referred to a
Systematic Reviews. 2014; 11: CD006904. regional weaning centre. Thorax. 2005; 60: 187–192.
Boles JM, Bion J, Connors A, et al. Weaning from Smith IE, Shneerson JM. A progressive care programme
mechanical ventilation. European Respiratory Journal. for prolonged ventilatory failure: analysis of outcome.
2007; 29: 1033–1056. British Journal of Anaesthesia. 1995; 75: 399–404.
Burns KE, Meade MO, Premji A, Adhikari NK. Vasilyev S, Schaap RN, Mortensen JD. Hospital survival
Noninvasive ventilation as a weaning strategy for rates of patients with acute respiratory failure
mechanical ventilation in adults with respiratory in modern respiratory intensive care units. An
failure: a Cochrane systematic review. Canadian international, multicenter, prospective survey. Chest.
Medical Association Journal. 2014; 186: E112–E122. 1995; 107: 1083–1088.
Damuth E, Mitchell JA, Bartock JL, Roberts BW, Trzeciak Weiss CH, Moazed F, McEvoy CA, et al. Prompting
S. Long-term survival of critically ill patients treated physicians to address a daily checklist and process
with prolonged mechanical ventilation: a systematic of care and clinical outcomes: a single-site study.
review and meta-analysis. Lancet Respiratory Medicine. American Journal of Respiratory and Critical Care
2015; 3: 544–553. Medicine. 2011; 184: 680–686.
MCQs
True or False (d) Critical illness myopathy
1. Factors associated with extubation delay following (e) Sedation
cardiac surgery include: 3. Patients who experience weaning failure:
(a) Increasing age (a) Are defined as requiring invasive mechanical ven-
(b) Male gender tilation for 3 weeks or more and following three or
(c) Anaemia more failed weaning trials.
(d) COPD (b) Account for fewer than 10% of patients treated
in ICU, but represent more than 30% of ICU bed
(e) Preoperative renal dysfunction occupancy
2. For patients who experience prolonged ventilation, (c) Rarely survive more than 12 months out of hospital
factors that may be associated with an increased
LOAD on the respiratory system include: (d) Represent an important but decreasing number of
ICU patients
(a) Excessive airway secretions
(e) Benefit from a stepwise reduction in pressure
(b) Obesity support
(c) The tracheostomy
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Section 8 Provision and Delivery of Cardiothoracic Intensive Care
Cardiothoracic Critical Care Nursing,

Chapter
53 Outreach and Follow-up

Jo-anne Fowles
Introduction their careers. The education team is able to ensure

all staff have access to appropriate educational
Caring for the critically ill cardiothoracic patient
opportunities.
requires a multidisciplinary approach with nursing
roles being pivotal. Nursing the critically ill cardiotho-
racic patient requires advanced skills and competence Bedside Nurse
as well as in-depth knowledge of nursing practice, Integral to the care of the patient is the bedside nurse.
anatomy, physiology and pathophysiology, technol- Their roles vary in different cardiac intensive care units
ogy and pharmacology used in critical care. Integral and countries, but they are the person who has the most
to the nurses’ role is supporting patients and their contact with the critically ill patient. The roles of the
families during and after critical illness. bedside nurse are summarised in Table 53.1. In criti-
Critical care areas are constantly adapting to the cal care this is a registered practitioner who enhances
needs of the patient and now often extend beyond the the delivery of comprehensive patient centred care, for
physical unit itself. The concept of ‘critical care with- acutely ill patients, often on a 1:1 basis. Structured hand-
out walls’ is well established and ensures continuity over at the start of each shift ensures accurate transfer
of the patient pathway before, during and after the of clinical information ensuring continuity of safe care.
ICU admission. Many units now further defragment The primary role of the bedside nurse is continu-
the care of the critically ill patient through advanced ous vigilance of the patient’s vital signs, recognising
nurse practice, developing the role of the healthcare and assessing changes and responding immediately.
support worker, establishing new ways of working and This response includes communicating with the nurse
offering nurse led services. in charge and the rest of the multidisciplinary team
(MDT) where appropriate.
The Nursing Team Many patients are invasively monitored. Setting
up, calibration and appropriate alarm limits to ensure
Education Team accuracy and safety of monitoring is the responsibil-
Most critical care area nursing teams include a dedi- ity of the nurse. The critically ill cardiothoracic patient
cated education team, their role being primarily to may also require advanced support ranging from
ensure access to all nurses to appropriate education continuous renal replacement therapy (CRRT) and
and to support the senior nursing team in sharing best intra-aortic balloon pump (IABP) to ventricular assist
practice. devices (VAD) or extracorporeal membrane oxygena-
Critical care is a complex specialty with the new tion (ECMO). Monitoring of the patient on these
nurse having to acquire many skills and competen- devices is the responsibility of the bedside nurse. In
cies. The education team provides both a framework addition to basic nurse education, critical care nurses
and support to meet these needs. Technology within have specialised training. This training includes set-
critical care is constantly evolving and the education ting up and ongoing management of monitoring
team has a vital role in ensuring all new equipment equipment and advanced mechanical support to
is introduced with a robust training programme to ensure patient safety.
ensure patient safety. It is important that all nurses are Assessing the needs and delivering basic nursing
provided with the opportunity to develop throughout care remains an essential component of the bedside
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Section 8: Provision and Delivery of Cardiothoracic Care
Table 53.1 Duties of the bedside nurse patients when necessary, whilst ensuring patient care
The bedside nurse’s plan of care on a daily basis will is never compromised.
include the following The role of the bedside nurse may vary between
Basic needs: units but regardless of differing degrees of autonomy,
• Assess all needs and provide general hygiene including eye central to the bedside nurse role is the ability to rap-
care, mouth care, bathing
idly respond to potentially life threatening conditions.
• Prevent self harm when patients are agitated
• Bowel care
Skin care: Health Care Support Worker/Assistant
• Regular repositioning to prevent pressure sore development
• Correct positioning of invasive devices to avoid skin damage
Practitioners
• Assessing skin integrity and use of appropriate dressings The value of the health care support worker role
and creams within cardiothoracic critical care is well recognised.
• Ensuring correct pressure relieving mattress utilised They are not registered, and when delivering patient
• Cleanliness to avoid development of moisture lesions care always work under supervision of the registered
• Assessing wounds and ensuring correct dressings used nurse. The role is evolving and expanding with foun-
Infection control:
dation degree pathways providing training in skills
• Ensure local infection control policies are adhered to
essential to delivering care and basic assessment.
• Recognise early signs of infection
Psychological support:
In addition to direct patient care they perform a
• Allay patients’ fears and concerns by ensuring they are variety of tasks essential to the smooth running of
comfortable, reassured and fully informed any unit. These include checking emergency equip-
Family care: ment, ordering supplies and cleaning and tidying the
• Ensure good communication and support family members clinical area.
Monitoring:
• Documenting and interpreting monitored parameters
and communicating concerns early to prevent further
Nursing Hierarchy
deterioration In the UK there are a variety of senior nurse roles
Medications: within cardiothoracic critical care. These may include
• Administering all prescribed medications all or some of the following:
• Titrate infusions within defined parameters (e.g. sedative
• Lead nurse;
infusions)
MDT: • Matron;
• Participate in MDT discussions acting as the patient’s advocate • Advanced nurse specialist/practitioner;
Rehabilitation: • Shift leader.
• Be involved in the planning of rehabilitation One or more of these roles may be filled by one indi-
• Assist with mobilising patients whenever possible vidual, for example the shift leader may also be an
Advanced support:
advanced nurse specialist or nurse consultant.
• Assisting with intubation
• Regular bronchial toilet in ventilated patients
Nurse Manager/Lead Nurse/Matron
• Care of tracheostomies including decannulation
• Monitoring and managing CVVH, plasmapheresis, IABP The critical care manager carries responsibility for
• Measuring cardiac output studies, documenting and service delivery, budgetary management, recruitment
interpreting results and communicating concerns and retention. Although all units vary they are usually
• Assisting with the insertion of invasive lines supported by senior clinical nurses or matrons.
• Monitoring the patients supported with ECMO and VADs The nurse manager’s role is multifaceted covering
management of staff, including appraisal and perfor-
mance management, handling complaints and inves-
nurse role. This includes communication with and tigating untoward incidents, and ensuring any lessons
support of both the patient and their family. Although learnt are shared with the entire team. They provide
the primary focus is the allocated patient, the nurse is leadership, ensuring that the nursing service is con-
part of a team delivering care and responding to the tinually evolving to provide the highest standards of
changing demands of the unit. This includes respond- patient care. This is achieved through working with
ing to unexpected events to allowing rapid turnover of the MDT supporting, developing and implementing
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Chapter 53: Critical Care Nursing, Outreach and Follow-up
policies. A strong commitment to education and or readmission to the critical care area. The nurse led
training, and involvement in research and audit pro- outreach team works closely with the ward and ICU
jects is also essential. staff to ensure this happens. The outreach team is
available 24 hours/day, 7 days/week.
Shift Leader The three essential objectives of an outreach team
The nursing team in the clinical area is led by a senior are as follows:
nurse or in larger units a team of senior nurses. The 1. Prevent readmissions by recognising and treating
role of the senior nurse in the clinical area is to main- the deteriorating patient, and if required, ensure
tain an overview of all patients. At the onset of each admission to critical care happens in a timely
shift, the senior nurse allocates nurses to patients, manner.
ensuring the most appropriate, safe and effective 2. Enable discharge from critical care by supporting
use of available skills. Consideration is also given to ward staff in the monitoring and management of
providing opportunities for nurses to develop skills this group of patients.
with adequate support. The senior nurse remains vis- 3. Share critical care skills, including recognition of
ible and available to the MDT, patients and relatives the deteriorating patient, with ward staff.
throughout the shift. The senior nurse is involved in Excellent communication and teaching skills are as
all MDT rounds. important to the outreach nurse as advanced clinical
The senior nurse role also includes the coordina- skills. Their role is to support and develop ward staff
tion of admission, transfer and discharge of patients. in identifying and managing the deteriorating patient.
Integral to the role is an awareness of infection status An effective outreach team will enjoy excellent team-
of all patients, with excellent infection control prac- work with ward staff, thus ensuring safe and effective
tice being important in preventing hospital acquired care post discharge from the critical care area.
infection. Many hospitals utilise an early warning system,
for example MEWs, to provide an early predictor of
Advanced Nursing Roles clinical deterioration. Such systems provide a trigger
Advances, developments and challenges in modern for ward staff to alert the outreach team of the dete-
healthcare provision result in a constantly chang- riorating patient so ensuring early intervention and
ing clinical environment. This is especially evident management.
in the cardiothoracic critical care area as this heavily
resourced setting continues to proactively respond to
deliver high quality, safe patient care. As a result there
Follow-up
is an ever changing face to critical care nursing. It is well recognised that patients can experience
Advanced nursing roles have developed in recent long lasting side effects after recovery from critical
years to improve patient care by ensuring immediate illness. Patients and their families need to be given
response and a less fragmented approach. The roles support in managing the psychological impact of
encompass many job titles, such as clinical nurse spe- their illness.
cialists, advanced nurse practitioners and nurse con- The support and follow-up needs of the cardiotho-
sultants. All of these roles enable the nurse to work racic patient post ICU and hospital discharge has tra-
with increased autonomy within specific guidelines, ditionally been met by the ‘parent’ team of cardiology,
following appropriate training and assessment. An surgery or transplantation. This is now changing with
example of this is that in many units management of many units providing follow- up immediately post
the immediate postoperative cardiac surgical patient ICU discharge and longer term.
is nurse led with advanced nurse specialists managing The impact, not only of a critical possibly life
ventilation, haemostasis, fluid and electrolyte balance threatening illness, but also the sensory overload in
and drug prescription within defined guidelines. the ICU and polypharmacy, including opiates, may
affect patients’ psychological recovery. Patients may
also suffer from sleep deprivation and periods of delir-
Outreach ium whilst in the ICU, both of which may impair long
The early identification of the deteriorating patient on term psychological recovery. Symptoms reported by
the hospital ward is crucial in preventing admission patients following an ICU admission include memory
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loss and/or memory gaps and nightmares that may • A well-organised education team is required to
continue after hospital discharge. ensure development and maintenance of essential
In addition to clinics assessing psychological skills.
recovery and offering specialist support, many car- • The development of advanced nurse specialist
diothoracic critical care units are introducing patient roles is required to ensure patients receive care
diaries. The diary is completed on behalf of the patient and intervention in a timely manner.
giving a day to day record of the admission to the ICU • An outreach team with excellent communication
and is a useful tool for helping fill in memory gaps and skills is essential to ensure ongoing care post ICU
promoting psychological recovery. discharge.
• Follow-up of patients by ICU teams is important
Conclusion in long term recovery.
Nurses have an integral role within the multidiscipli-
nary team in providing skilled, advanced care of the Further Reading
patient in cardiothoracic critical care. The recognition
Galley J, O’Riordan B. Guidance for Nurse Staffing in
that care of the critically ill patient extends beyond
Critical Care. Royal College of Nursing (RCN).
the boundaries of the intensive care unit has led to the 2003. www.rcn.org.uk
development of nursing roles to ensure early detection
Jones C, Griffiths R, Humphris G, Skirrow P. Memory,
and supportive follow-up of all patients. delusions and the development of acute post-traumatic
stress disorder-related symptoms after intensive care.
Learning Points Critical Care Medicine. 2001; 29: 573–580.
• Communication and collaborative working are
central to safe, effective patient care regardless of
each unit’s nursing strategy or patient pathway.
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Systems and Processes in Cardiothoracic

Chapter
54 Critical Care
James Moore and Alain Vuylsteke
A cardiothoracic critical care unit is a highly complex be developed for a wide range of situations within
environment requiring an interplay of multiple medi- critical care.
cal specialties and allied health professionals involved A bundle is defined by the Institute for Healthcare
in the care of those patients recovering from the insult Improvement (IHI) as a structured way of improving
caused by cardiac surgery. Most of these units will the processes of care and patient outcomes: a small,
treat patients suffering from any organ dysfunction straightforward set of evidence-based practices –gen-
that happens in addition to cardiorespiratory issues. erally three to five –that, when performed collectively
In general, systems and processes will be similar to and reliably, have been proven to improve patient
those used in any critical care unit. outcomes.
There is very limited room for error in this highly Advantages and criticisms of care bundles are
dynamic environment. The complexity of the patients’ listed in Table 54.1.
needs has driven the development of standardised Bundles have now been developed for a wide
pathways and protocols to improve outcomes and range of clinical scenarios in the critical care unit.
maximise efficiency. This is supported by the increas- An example of a widely adopted bundle of care is that
ing demand by the public and regulatory authorities developed for the prevention of central line associated
to provide treatment and support in an environment bloodstream infections (CLABSI) promulgated by
that operates within a structured framework. the IHI and is shown in Table 54.2. Implementation
of the central line bundle in the state of Michigan,
Guidelines and Protocols USA resulted in a 66% reduction in CLABSI over an
The past 10 years has seen an explosion in the num- 18 month period.
ber of guidelines and protocols available to the critical Bundles are designed to be adopted as a full pack-
care clinician to aid the management of the individual age rather than being taken up as single points in a
patient. This has been facilitated by how easy it is now piecemeal approach. It is essential that they are regu-
to share electronic documents. larly reviewed, as some elements of the bundle may be
A clinical guideline is a systematically developed subject to new research findings –an example being
statement to assist practitioner and patient decisions intensive blood glucose control, which was included
about appropriate health care for specific circum- for a time in ICU care bundles, but has subsequently
stances. Protocols tend to be a more prescriptive been shown to be associated with higher mortality
set of instructions for the management of a specific than more liberal targets.
condition.
The publication of Rivers’ Early Goal Directed Multidisciplinary Team Input
Therapy study in 1999 popularised the development The care of patients in the cardiothoracic critical
of bundles in critical care. This study showed that the care unit benefits from the input of multiple medical
use of a specific bundle of care for the management of specialists and allied health professionals. Complex
severe sepsis in a single centre significantly improved patients often suffer from multiple medical comorbid-
mortality. Although the study has been subsequently ities, and complications following surgery can affect
exposed to significant criticism, bundles began to almost every organ system.
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Table 54.1 Advantages and criticisms of care bundles
Advantages of care bundles Criticisms of care bundles

Standardisation between patients May not take into account individual patient
Evidence of improved patient outcomes when bundles are used May limit individual clinician’s autonomy or independence
Promote efficient use of resources by utilising proven and An unintended side effect of standardisation may be that it
effective interventions discourages excellent or exceptional clinical practice
Can potentially limit fringe practices which may be unproven or May be unduly influenced by external forces such as government or
dangerous (and frequently expensive) industry
Some individual bundle elements may have limited evidence; and
evidence may change with time
Result in additional administrative burden for staff
accountable for continually improving the quality of

Table 54.2 Example of care bundle
their services and safeguarding high standards of care
Central Line Bundle by creating an environment in which excellence in
Hand hygiene clinical care will flourish.
Maximal barrier precautions The cardiothoracic critical care unit requires
Chlorhexidine skin antisepsis a strong focus on clinical governance, to ensure
Optimal catheter site selection –avoidance of using the femoral
patient safety, and continuous improvement in qual-
vein for central venous access in adult patients ity of care. The key elements of clinical governance
Daily review of line necessity with prompt removal of as published by the National Health Service (NHS)
unnecessary lines in England can assist in ensuring a comprehensive
programme of quality improvement is in place within
There has been extensive research in the general individual units.
critical care setting into the relative merits of ‘open’ One approach to developing a robust structure of
versus ‘closed’ units. ‘Closed’ units have the care clinical governance is to consider the so-called ‘pillars’
directed by specialists in critical care medicine who of a clinical governance as shown in Figure 54.1.
call on other teams as required. ‘Open’ units allow
the primary team to admit and direct the care with Clinical Audit
(or without) support from critical care specialists. Clinical Audit involves a systematic analysis of an
Complex patients may benefit from a shared model area of practice to improve clinical care and/or health
of care; however conflict over management strategies outcomes, or to confirm that current management
and goals of care can easily emerge. is consistent with the available evidence or accepted
A close and constructive working relationship guidelines. Audit has become a core skill expected of
between all teams, with clear and open communica- health professionals, and can act as an important tool
tion, are essential to ensure the system works well for to drive improvements in quality of care.
the patient. The ‘audit cycle’ describes a widely accepted
Most surgical patients admitted in cardiotho- approach to undertaking clinical audit activities. After
racic critical care will move from a very high to a first identifying a topic to audit, accepted standards
low level of dependency within a few hours. Such are clearly defined. Current practice is then measured
patients can be managed in a nurse led unit according and compared to those standards. This is then com-
to predefined pathways with minimal medical input. municated to the team, a plan for change designed and
However, complex patients require input from a wider implemented, and finally re-audit should take place to
multidisciplinary team. examine how those changes have influenced practice.
Clinical Governance Clinical Effectiveness

Clinical governance encompasses a variety of meas- Critical care is now firmly in the era of evidence-
ures designed to ensure that health organisations are based medicine, and there is a vast array of literature
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Chapter 54: Systems and Processes
encouraged to identify and report risk (both clini-

Education cal and non-clinical), and the department needs to
and have tools to manage and minimise this risk. Critical
training care remains a human endeavour and so errors will
Risk Clinical always be expected to occur –an effective risk man-
management audit agement system understands this, but strives to pre-
vent and minimise any harm that occurs as the result.
Clinical When errors do occur, reporting needs to be strongly
governance encouraged so that learning can take place, and sys-
tems examined to try and prevent similar events
Clinical
Openness occurring in the future. Staff need to feel reassured
effectiveness
that in reporting actual or potential (‘near-miss’) inci-
Research dents, they will be supported –a ‘no-blame’ culture is
and essential for staff to feel safe to report. Equally, inves-
development
tigation of events should be undertaken in a struc-
tured, fair and open manner by trained staff. The aim
of an accident investigation is not to assign blame, but
Figure 54.1 Pillars of clinical governance. Extracted from College to determine what can be done to prevent the event
of Intensive Care Medicine IC-8: Guidelines on Quality Improvement. occurring again in the future. Regular mortality and
morbidity review meetings are another important
examining new concepts and re- examining estab- component of a system wide risk management pro-
lished practices. Clinical effectiveness requires con- gramme. These meetings should ideally be multidisci-
sideration of health economics and ensuring that best plinary, including trainee involvement, and involve a
value for money is obtained. thorough review and discussion of patient complica-
The College of Intensive Care Medicine in Australia tions, adverse events and deaths. Action points should
and New Zealand recommends examining three broad be minuted and progressed.
types of outcome measures as listed in Table 54.3. Risk management can frequently be seen as only
Critical care units should participate in pro- examining negative events, but learning from good
grammes that measure the effectiveness of the care performance is equally important. Identifying and
they provide. A number of professional societies in publicising examples of excellent practice can help
intensive care around the world run audit and qual- to drive positive culture change as much as learning
ity assurance programmes whereby individual units from negative events.
submit patient outcome data which are then ana-
lysed and compared to similar units. A number of Openness
outcome measures are able to be calculated, includ- Learning from instances of both good and bad practice
ing the standardised mortality ratio (SMR), which requires a culture of openness where these events can
compares actual mortality rates to those predicted by be discussed in a constructive and meaningful way.
tools such as the APACHE-III (Acute Physiology and Increasingly, the health system is moving to a cul-
Chronic Health Evaluation III), and exponentially ture of open public reporting of serious adverse events,
weighted moving average (EWMA) charts which may as well as reporting outcomes and quality measures.
allow early identification of developing trends. These Cardiothoracic surgery was one of the pioneering spe-
outcome measures will usually have a process for cialties in this field and has well-developed systems in
identifying poorly performing ‘outlier’ units, allow- place for public reporting of surgical outcomes.
ing investigation of cause and provision of support to ‘Dashboarding’ is another developing area where
improve quality of care. key quality measures are made available in real time
in an easy to follow graphical format. This can allow
Risk Management all members of the team to see the unit’s achievements
An effective risk management system requires both over a range of key performance indicators –the infor-
proactive and reactive elements. Staff should be mation can be made public, for example via a website.
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Table 54.3 Three broad types of outcome measures groups have formed with the aim of producing high
recommended by the College of Intensive Care Medicine in quality multicentre clinical trials in critical care medi-
Australia and New Zealand
cine. These include the Canadian Critical Care Trials
1. Structural measures Examples: Group, the Australia & New Zealand Intensive Care
Size of the ICU
Society Clinical Trials Group and the UK Intensive
Whether the ICU is open or closed
Care Society, as well as many others.
Type or amount of technology
available
Number and roles and Conclusion
responsibilities of ICU staff Developing a safe and effective culture within car-
Clinical workload and case mix
diothoracic critical care requires multidisciplinary
Levels of trainee supervision
involvement in patient care, and the use of vali-
2. Process measures Examples: dated protocols and bundles of care, especially in
Rate of DVT prophylaxis
the management of high risk conditions or techni-
Rate of stress ulcer prophylaxis
cal procedures. The seven pillars of clinical govern-
Early enteral feeding
Delayed discharge from ICU
ance provide an excellent structure for considering
Appropriate transfusion threshold the essential elements of care, processes and qual-
Blood glucose control ity within the ICU. Although often seen as ‘back-
Hand hygiene ground functions’, these elements are essential to
Time to administration of providing the highest quality of care to the indi-
antibiotics vidual patient.
Lung protective ventilation
strategies
End of life management Learning Points
3. Outcome measures Examples • Cardiothoracic critical care is a highly complex
Severity adjusted mortality rate environment requiring input from multiple
Health related quality of life health professionals.
Unplanned ICU readmission • Standardised pathways and protocols have been
Serious adverse drug event rate developed to improve outcomes and maximise
Ventilator associated efficiency.
pneumonia rate
Central line associated
• Cardiothoracic critical care requires a strong
bloodstream infection rate focus on clinical governance to ensure patient
Family satisfaction safety and quality improvement.
• Risk must be actively managed and organisations
should develop a culture which encourages the
Research and Development team to report when things have gone wrong.
• Learning from incidents should be incorporated
Medical research is essential for the ongoing advance-
into practice and clinical outcomes made
ment of the specialty. This includes research into
available to the public so as to drive
basic science, new innovations or technology, and re-
improvements in performance.
examining traditional ideas and thinking (or medical
dogma).
Research can drive improvements in quality and Further Reading
safety, such as the development of care bundles men- Scally G, Donaldson LJ. Clinical governance and the drive
tioned previously in this chapter. Medical research has for quality improvement in the new NHS in England.
traditionally been driven by individual researchers, British Medical Journal. 1998; 317: 61.
but over the last 20 years a number of collaborative
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Clinical Information Systems

Chapter
55 Matthew Jones
Introduction Different systems vary too in the degree to which

they can be customised to local requirements. Some
Critical care is a highly data intensive environment. It
offer relatively little flexibility and require adopting units
has been estimated that over the course of a 24 hour
to adapt themselves to the ways of working envisaged by
period nearly 1500 data items may be documented on
the CIS designers. This simplifies CIS implementation
a typical critical care patient and this volume of data
and may therefore be attractive to hospital IT depart-
is growing all the time. Historically, a subset of these
ments, but may provoke resistance from critical care
data would have been transcribed into a paper-based
staff who are required to adjust their work practices.
record, which was not always legible, could some-
At the other extreme, systems may be highly customis-
times go missing and was difficult to analyse. Under
able, either by the vendor, or by the users. This is likely
these circumstances the emergence of clinical infor-
to make the system more attractive to clinical staff, for
mation systems (CIS), computer-based systems that
example, if displays can be made to appear similar to
collect, store, manipulate and display clinical data, has
those of the paper or electronic systems the CIS replaces,
been widely identified as offering significant benefits
but incurs additional costs and creates idiosyncratic sys-
to healthcare delivery in critical care. While there is
tems, the integration of which with other services may
evidence that CIS can contribute to improvements in
be problematic. In practice, moreover, there will be lim-
patient care, they also pose new challenges. A balanced
its to the extent to which systems can be customised and
appreciation of their capabilities and their effects on
certain aspects of the CIS may be so deeply built into
clinical work practices is therefore necessary.
the design that changing them may be impractical. This
can sometimes cause problems where CIS developed for
The Components of a CIS one particular health system are imported to another.
There is no universal model of a CIS and often the Nevertheless, even relatively superficial customisation,
configuration in a specific critical care unit will reflect such as changing screen colours, adding a logo or pre-
the particular combination of hardware and software senting a familiar screen as the default may be signifi-
installed locally. On the software side, early CIS in cant in influencing user acceptance.
critical care tended to be bespoke developments, but In terms of hardware, a CIS generally comprises a
now there is a wide range of commercial systems server, hosting the central database, and client com-
available, either as specialist modules of general hos- puters, at the bedside or elsewhere, accessing the data
pital information systems, or standalone products over a network. Client computers may be desktops,
designed specifically for intensive care settings. The laptops, tablets or other mobile devices. ‘Thin’ clients,
former have the advantage of full integration with which may run on relatively cheap and low powered
other specialisms, ensuring that critical care episodes devices, simply provide a view of data that are held
are documented in a way that is consistent with prac- and processed on the central server, while ‘thick’ cli-
tice elsewhere in the hospital, but may not be optimal ents, which require more powerful computers, carry
for the particular requirements of critical care. The out processing locally and only exchange data with
latter are likely to fit better with critical care practices, the server. Thick clients may be more reliable than
but may not exchange data seamlessly with other hos- thin clients as they are not so vulnerable to network
pital systems. Hospital IT departments may also be or server failures, but are more expensive to purchase
reluctant to support more than one system. and operate (Figure 55.1).
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Figure 55.1 (a) Thin and (b) thick clients.
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Chapter 55: Clinical Information Systems
Although, in principle, a CIS integrates all patient ward rounds’ in which staff meet in an office to review
data, in practice hardware constraints can mean that the patients’ CIS records rather than visit each bed-
some elements of patient data may not always be side. Although this may allow for more focused dis-
incorporated. This may be due, for example, to the cussion with fewer disruptions, it reduces interaction
lack of compatible interfaces to enable critical care between clinicians and patients and bedside staff that
equipment to communicate with the CIS, or due to may be significant for clinical decision making and
the resolution of screens being insufficient to display patient welfare.
X-rays in sufficient detail. While the vision may be of While the standardisation and centralisation of
a unified repository of all clinical data, therefore, this data and their easier availability may be a key feature
may not always be achieved. Nevertheless it is possible of CIS, further advantages may be gained from func-
to identify a CIS as comprising a number of compo- tionality that makes use of the data. One area that
nents that are present to a greater or lesser degree in has received particular attention is that of electronic
most systems. prescribing (Figure 55.2), where the CIS may provide
The core component of a CIS is an electronic med- new functionality such as: presenting pre-filled order
ical record, a database containing a variety of forms sets, for example of the drugs typically administered
of data about patients. Many of the data fields will be on postsurgery admission to critical care; restricting
numeric, for example recording blood pressure or prescribed dosages within preset upper and lower
heart rate, and therefore readily capable of manipu- bounds; or checking prescriptions against allergies
lation and analysis, but others may contain text, for or interactions with other medications. With remote
example clinical notes, that are less easily analysed. access it is also possible for a pharmacist to review
There is a tendency for CIS to support numeric data medication without needing to visit the bedside, or
entry in preference to free text, and thereby to pro- even the unit.
mote a more systematic and standardised approach It is not just in prescribing that a CIS may sup-
to recording clinical care. Textual data may be transport clinical practice. Some systems may include
lated into numbers, for example by offering a pick functionality to monitor the patient’s condition and
list of common options to be selected from (option1, treatment and alert clinicians to potentially signifi-
option2. … , optionn), while perhaps retaining the cant correlations, or remind them when actions have
possibility of free text entry for non-standard cases. not been taken. Many also support checklists to guide
Electronic records also avoid problems of legibility of and improve care. Such clinical decision support is
text entries and identify unambiguously who has writ- not a necessary feature of a CIS, however, and may
ten them (as individuals need to log in to the CIS to be be perceived by some clinicians as intruding on their
able to enter data). autonomy. Care is also needed to ensure that alerts are
With data transferred directly from medical equip- relevant and not so frequent that they are ignored.
ment to the CIS, transcription errors (which may be Another potential contribution of CIS to clinical
of the order of 20%) are eliminated and recording is practice is in the display of data in new ways. Some
no longer dependent on staff availability (although it individuals or professional groups, for example, may
may be necessary for them to validate the data occa- prefer to view data graphically, while others may pre-
sionally to ensure that erroneous data do not contami- fer to focus on specific values. A CIS can enable mul-
nate the record). Numerical calculations, for example tiple views of the same data, matched to individuals’
of fluid balances, are also automated, thus avoiding preferences. The potential for immediate access to all
another potential source of errors. Once in the data- a patient’s data, not just, as was the case with paper
base, moreover, the data are permanently stored and records, those from the past 24 hours, also enables
immediately retrievable, not just at the location where clinical staff both to view trends in particular values
they were entered. Data should therefore no longer over any period and to zoom in on specific data points
get lost, and may be accessed away from the bedside anywhere in that time series. The CIS thus provides
at any time by any authorised person. With suitable both additional dimensionality and granularity to the
secure networks, this access may potentially be from data available for clinical decision making. Different
locations distant from the patient, creating the oppor- CIS vary, however, in the flexibility they offer to users
tunity for remote supervision and teleconsultation. in the ways that data are presented. Some have a rela-
Remote access may also encourage the use of ‘sitting tively limited menu of standard views, while others
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Figure 55.2 Electronic prescribing.
give users a high degree of control both on how data implementing a CIS. It is estimated, for example, that
are presented and on what particular data items are the five years cost of ownership of major computer
displayed. More advanced CIS may support dynamic systems can be five to eight times the initial outlay.
views, allowing health professionals to bring together Some of the more significant items contributing to
different blocks of data on the same screen as relevant this cost include: infrastructure, for example cabling
for each individual patient. and networks; interfaces (to enable the CIS to receive
Over time, the accumulation of historical data in data from medical devices, perhaps requiring some
a CIS database can become a significant resource for of them to be updated); project management of the
care quality improvement, audit and research. The implementation process; customisation (to adapt the
standard tools provided with many CIS, however, system to local practices); training (both the recruit-
do not always make it easy to extract data and this ment or secondment of staff to deliver the training
resource is often underused as clinical staff lack the and the time for staff to undertake it); and initial
time and expertise to undertake the task. Reuse of loss of staff productivity as they learn to use the CIS.
data may also be discouraged by time and resources Nor are costs restricted to the initial implementa-
required to ‘clean’ and/or process the data before they tion –hardware maintenance and upgrading, soft-
can be analysed. Although offering great potential, the ware license fees and updates and ongoing training
contribution of CIS to data led healthcare practice and (of newly recruited staff and of existing staff if new
policy may therefore be less than some current propo- functionality is added) mean that there is a continu-
nents of ‘Big Data’ envisage. ing outlay.
Given these costs, there is likely to be, not unreason-
ably, an expectation that the CIS will deliver significant
Costs and Benefits of a CIS benefits. Some of these may be direct savings: through the
The direct expenditure on hardware and software elimination of tasks, such as processing of paper records,
constitutes only a small proportion of the cost of that the CIS makes redundant; through efficiency
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gains, for example staff being able to review the status although CIS may contribute to some new errors,
of a patient without needing to visit the bedside; and such as selecting the wrong item from a pick list,
through the elimination of costs (e.g. purchase, storage) in general, the legibility, availability and account-
associated with paper records. It is often assumed that ability of electronic records along with error checks
an important benefit of a CIS will be in time saving, for and alerts contribute to a reduction in medication
example through the elimination of data transcription. errors. Despite the difficulties that may be encoun-
In practice, however, while CIS use undoubtedly speeds tered in extracting data, moreover, CIS can enable
up certain tasks, evidence suggests that CIS rarely frees fine-grained analysis of critical care practice to sup-
up significant time overall as other tasks, such as data port service improvement, audit or research. Other
entry with a keyboard, take considerably longer than indirect benefits may be less tangible, but successful
with pen and paper. What a CIS can provide, though, are adoption of a CIS can contribute to improvements
better data to enable cost management. in staff morale and unit reputation (with potentially
It is perhaps the indirect benefits of a CIS that positive effects on staff turnover). See Table 55.1 for
have the greatest impact on critical care. For example, a summary.
Table 55.1 Costs and benefits

Main costs associated with the implementation of a CIS
Direct initial purchase costs Hardware purchase and installation
Software purchase/licence, customisation and installation
Infrastructure purchase and installation
Indirect initial purchase costs Replacement or upgrade of equipment to interface with the CIS
Direct recurrent costs Hardware maintenance, repair and upgrade costs
Software licence/upgrade costs
Consumables
Direct initial staff costs Project management
Staff time for customisation
Recruitment and employment of trainers
Staff time during training
Direct recurrent staff costs User support
Ongoing training
Ongoing customisation
Data extraction
Indirect staff costs Initial loss of productivity
Management time
Staff resistance/turnover
Main benefits associated with the implementation of a CIS

Direct savings Elimination of costs and tasks associated with paper records
Efficiency gains in certain tasks
Indirect benefits Improved legibility of records
Improved availability of records
Improved accountability for data
Clinical decision support
Data to support cost management, audit and research
Improved staff morale
Improved unit reputation
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As may be evident, the adoption of CIS in criti- review of any individual’s practice. Even if this func-
cal care is not solely a technical exercise, but requires tionality is never used, some users may be uncomfort-
careful and effective leadership and management. It able with the prospect that their work may be subject
is generally recognised that this leadership needs to to continuous surveillance. The association with a par-
be clinical rather than managerial, both to ensure that ticular username depends, of course, on individuals
the CIS is aligned with a clear clinical vision, but also only logging into the CIS under their own name. Even
to act as a credible ‘champion’ able to motivate and making this a mandatory requirement, with discipli-
persuade others through what can sometimes be a nary consequences for non-compliance, may not be
trying process. enough to prevent some, especially senior, users who
consider that data entry is not a good use of their time
or expertise, from finding ways to circumvent it, for
Effects of CIS on Clinical Practice example by getting colleagues to enter data for them,
The objective of introducing a CIS in critical care or sharing their login credentials. Notwithstanding
is not to install yet more equipment, but to support such efforts, the clear accountability for actions that
and enhance clinical practice. The extent to which a a CIS creates would seem a reasonable expectation of
CIS achieves this, however, will depend on its ability good clinical practice.
to support clinical workflows. Where a CIS is poorly While it is not a necessary feature of a CIS that
aligned with the way in which staff carry out their work practices are standardised (for example, systems
tasks, for example by introducing additional stages to can be designed to allow data entry in a variety of for-
activities carried out under time pressure, they may mats), a CIS can be perceived as promoting greater
be reluctant to use it, or, where use is mandated, may standardisation of care, for example by providing
look for workarounds that will ‘keep the CIS happy’ protocols and order sets that make it easy to follow
with the minimum disruption to their work. This can best practice. This may be considered a good thing in
lead to the persistence of unofficial, often paper-based many respects, ensuring that care tends to conform to
work practices, discrepancies of which with the CIS a common evidence-based standard, but may be con-
record can be a potentially serious source of errors. sidered constraining by some clinicians. On the other
It also means that the CIS record may be incomplete, hand, this standardisation may be welcomed by new,
inaccurate or out of date and that capabilities offered temporary and junior staff, for whom the cognitive
by the CIS are only partially utilised. A CIS that has load of learning a unit’s distinctive practices is thereby
been designed with significant user involvement to reduced (although at the cost, some might argue, of
ensure that it facilitates rather than disrupts clinical excessive dependency on the CIS, which may cause
workflows, however, is more likely to enable benefits problems if it ever goes down).
to be effectively realised. A further concern with use of a CIS may be data
This is not to say, though, that some changes to overload. The volume, detail and depth of data that
clinical workflows may not be an intended and benefi- may be accessed may be seen by some clinical staff as
cial effect of CIS adoption. For example, where clini- overwhelming, and may make it hard to distinguish
cians have developed unreflective routines that do not the vital few data points from the less critical many.
conform to emerging best practice, the CIS can be an Studies also suggest that in most circumstances phy-
opportunity to review these and to support the adop- sicians are highly selective in the data to which they
tion of new protocols. Some staff may consider this pay attention, for example considering perhaps only
as restricting their clinical autonomy, and it may be a handful of items on every occasion that a patient is
necessary to allow them to override system defaults to admitted to critical care and never using a substantial
avoid resistance. If the new protocols are made easy to portion of the available clinical data. To a degree, how-
follow and can be shown to deliver benefits, however, ever, this is a problem that can be addressed through
then their use may become less contentious with time. appropriate data display, ensuring that critical values
Another aspect of CIS that may provoke concern are prominently visible, but having additional detail
from clinicians is what is sometimes referred to as its available when requested.
‘Big Brother’ effect. Because all actions taken with a Looked at from another perspective, however, the
CIS are time stamped and associated with a specific volume of data accumulated with a CIS can be consid-
user name, this creates the possibility for retrospective ered to offer a number of exciting new opportunities. It
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provides a more detailed, longitudinal and easily search- number of benefits over traditional paper-based records.
able record of a patient’s stay in critical care than has Automating documentation, for example, can eliminate
previously been available. This can be used to enable sys- transcription errors. A repository of all data relating to
tematic exploration of trends and relationships across a a particular patient, and across the whole population of
large population of patients, rather than just focusing on patients passing through critical care, can be built up and
the immediate care of the individual. At the same time made continuously and immediately accessible at the
it may also be used to personalise care for an individual, point of care. These data can be analysed and displayed
based on their specific characteristics, rather than rely- in a variety of ways according to clinicians’ preferences.
ing on standard values. Making best use of the opportu- Data can be analysed automatically to alert clinical staff
nities provided by a CIS to support a data led approach to significant interactions. Over time a data resource will
to care that does not lose sight of the individual patient be developed that can support audit and research. This
or of the importance of doctor–patient interaction, is process is not without its complexities and potential dif-
not straightforward, but is potentially one of the more ficulties, but provided that these are handled sensitively,
significant effects of CIS in critical care. Achieving this CIS can make a positive contribution to critical care.
will require strong clinical leadership to ensure that
opportunities are identified and that unit work practices Learning Points
and CIS design both support such an approach. • Critical care is a highly data intensive environment.
• CIS can support healthcare delivery in
Conclusions critical care.
The volume of data that is documented on critical care • Benefits of CIS include ready access to legible
patients would now seem beyond the capability of staff to patient records and electronic prescribing.
record by hand, or of paper-based records to adequately • CIS can however be costly to install and maintain.
represent in ways that can be used by clinicians. Deploying • Over time CIS can provide a powerful data
the power of modern computers to support this process resource to support audit, quality improvement
would therefore seem a sensible move. It also offers a and research.
MCQs
1. How many data items may be documented for an aver- (c) Improved computer literacy of staff
age critical care patient in 24 hours? (d) Staff savings
(a) 200 4. What proportion of the initial purchase cost of a
(b) 1000 major computer system does the five year cost of own-
ership amount to?
(c) 1500
(a) 10–20%
(d) 10,000
(b) 50–100%
2. What is the core technical component of a CIS?
(c) 500–800%
(a) A database (d) 1000–2000%
(b) A bedside computer 5. CIS adoption is more likely to be successful if led by:
(c) The Internet (a) Hospital IT experts
(d) A power socket (b) The CIS vendor
3. Which of the following is a generally recognised (c) External consultants
benefit of CIS? (d) A senior clinician
(a) Time saving
(b) Reduction in medical errors
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Medical Law and Ethics in the

Chapter

Oana Cole
The specialty of intensive care has evolved signifi- • In order to make a decision, the patient needs
cantly since its inception, approximately 50 years ago. to have the capacity to consent or not to the
With further advances in the field and the develop- treatment proposed.
ment of subspecialist branches, the complexity of We have introduced two further concepts here, con-
patients is increasing. A beautiful metaphor of the sent and capacity, which will be explained later.
‘modern patient’ is offered by the main character in
Philip Roth’s novel, Everyman, who contemplates ‘…
time having transformed his own body into a store-
Beneficience
house for man-made contraptions designed to fend All clinical actions taken must be to the benefit of the
off collapse.’ The flipside to that has been the increas- patient. In other words, if the patient cannot make
ing intricacy of medical law and ethics. In this chapter a decision, the healthcare professionals must act in
we propose to present some of the main issues briefly. accordance to the patient’s best interests.
The interested reader will find a short list of further
reading material at the end of the chapter. Non-malfeasance
Also known as primum non nocere, it is probably the
oldest and possibly the most controversial principle.
Ethics Principles Intensive care is characterised by very invasive, painful
While there are a number of ethical models, which procedures, which sometimes carry substantial risks.
have been applied to medicine in general and to criti- Should we stop doing them altogether? Certainly not,
cal care in particular, the most commonly taught one but we should consider the harm versus benefit of
is the Beauchamp and Childress approach. The four each manoeuvre. In other words, we need to balance
principles described act as a general guide to most beneficience and non-malfeasance.
aspects of patient care:
1. autonomy
2. beneficience Justice
3. non-malfeasance Most commonly this principle has been associated
4. justice. with the fair distribution of resources. While at organ-
isational level this translates into resource allocation
over a certain length of time, at individual patient level
Autonomy it is even more controversial. It underlies the issue of
It can be argued that autonomy is the first among equals. the last bed in the ICU or the long-term patient who
The patient is owed the respect for his/her own decision is unlikely to get better but who is using up precious
making. It is intended to counter the old attitudes of resources. In other words, cui prodest?
medical paternalism and support the patient in their
choices. There are two aspects that we must note here.
• It does not have any bearing on the wisdom of a
Consent and the Mental Capacity
decision; in other words, we cannot say that the Act 2005
patient’s decision cannot be respected simply The Good Medical Practice Guide published by the
because it appears to be unwise. GMC in 2013 stipulates that doctors should work
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Chapter 56: Medical Law and Ethics
in ‘partnership with the patients, sharing with them patient; the ‘reasonable’ doctor would be acting
information they will need to make decisions about in accordance to the practice of a group of peers,
their care’. This means that patients should consent to provided there is a logical basis for the practice.
intensive care. But how do we define intensive care? • The Chester v. Ashfar case moved the standard
Here are some of the aspects that may be important even higher, to explicitly offering information
to consider: that a reasonable patient would want to know.
• Intensive care is a process, rather than a The latter principle is usually explained as serious
geographical location; and common risks of a treatment or procedure.
• Various healthcare professionals are involved, However, it is necessary to consider the individual
each with a different impact on the patient’s patients as well –consenting a soprano or a
autonomy and dignity; chorister for intubation or tracheostomy is
• The degree of ‘burdensomeness’ of the critical different to consenting an engineer to the same
care process is individual to each patient; procedure.
• To date, there is not an accurate prognostic • Following the case of Montgomery v Lanarkshire
score for mortality or post-ICU morbidity; most Health Board, doctors must now ensure that
of the scoring systems have been validated for patients are aware of any ‘material risks’ involved
populations, not individuals; in a proposed treatment, and of reasonable
• There may be significant decrease in a person’s alternatives.
quality of life following an intensive care
admission; there are indications that the Patients Who Lack Capacity
more prolonged and complex the critical care
The procedure for patients lacking capacity is more
treatment, the more protracted the recovery to
complex. There are several possible solutions.
near premorbid condition.
1. The patient has an Advanced Directive (AD).
2. The patient does not have an AD; the healthcare
Patients Who Have Capacity professional should act in the patient’s best
Consent implies a two-way exchange of information interests.
between a doctor, or other healthcare professional,
3. There is disagreement amongst the
and the patient. The latter will have to demonstrate
multidisciplinary team members or between the
that they are capable of retaining and processing the
medical team and the patient’s family with regards
information given and communicate their decision
to what constitutes the best interests:
whether to accept or reject the treatment proposed, or
even not to make the decision until a later date. This (a) for long-term ICU patients, a court decision
would demonstrate that they have capacity, as stipu- should be sought;
lated by the Mental Capacity Act, 2005. (b) for short-term and intermediate-term
Note that the Act stipulates that capacity is issue patients, an Independent Mental Capacity
specific. Advocate (IMCA) should be consulted.
Consent is the legal counterpart of a patient’s The Mental Capacity Act has given more importance
autonomy. If the patient is temporarily incapacitated, to the AD than previously. However, there is a pleth-
as most of the ICU patients are, then either the deci- ora of cases in the medicolegal literature which prove
sion should be postponed until the patient recovers that there are multiple ways in which an AD is not
capacity, or other pathways of finding the best solu- applicable in a particular situation, especially in criti-
tion should be followed. Importantly, respect for the cally ill patients.
patient’s autonomy should also be shown in the way
the consent procedure is followed. What would the
patient like and need to know about the treatment Best Interests
proposed? There are a few guiding principles. The best interests test aims to canvass information
• The Bolam test with the Bolitho amendment – regarding the patient’s current and past views, as well
the information provided should be what a as the views of the relatives and the next of kin’s. For
‘reasonable’ doctor would disclose towards a example, it can be fairly safely predicted that a member
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of the Jehova’s Witnesses denomination would refuse a limitations of treatment are usually applied when
blood transfusion even if it were life saving. However, ‘we are hoping for the best but expecting the worst’.
there have been cases where a former Jehova’s Witness • DNAR –an order usually put in by a senior
had been given a blood transfusion if proven that he/ clinician to not start cardiopulmonary
she were no longer an active member of the denomi- resuscitation (CPR) on a patient in the event of
nation. HE v A Hospital NHS Trust (2003) is a prime cardiac arrest; most DNAR orders are initially in
example of such a case. place for 48 or 72 hours and the critical care team
Another important point is that should a patient are advised to revise the decision at the end of the
choose to refuse treatment, his/her wishes should be specified time period. It is appropriate to make
respected; however, should they insist on a treatment, a DNAR when the patient’s heart is not likely to
the doctor has the legal right to refuse based on clini- restart, or when there is no benefit in doing so.
cal grounds. All the principles enumerated above have been subject
to numerous ethical and legal debates and are likely to
Deprivation of Liberty
remain so, given the nature of the decisions involved.
Article 5 of the Human Rights Act states that ‘everyone Importantly, following a landmark judgement in 2014
has the right to liberty and security of person’. Persons, (Tracey v Cambridge) there is a presumption in favour
without capacity, who are under continuous supervi- of patient involvement in the DNAR decision mak-
sion and not free to leave the place where they are being ing process and if they lack capacity, their family and
treated are deprived of their liberty. Every patient admit- carers. It should be remembered that whilst active
ted to intensive care should be considered at risk of dep- treatment may be withheld, withdrawn, or a DNAR
rivation of liberty and those that are unable to consent decision may be put in place, patient care is never
should be referred for an urgent Deprivation of Liberty withdrawn or withheld.
Safeguards (DoLS) authorisation. Once in place, the
supervisory body will appoint a representative for the
patient, and ensure regular review as to whether ongo- The Diagnosis of Death
ing deprivation of liberty is required and remove the There are many definitions of death. A layperson will
authorisation when it is no longer necessary. All deaths have a certain concept of death, which will have a basis
of patients which occur where a DoLS authorisation is in the cultural and social characteristics of the group
in place should be reported to the coroner. they belong to. In a multifaith society, as are now most
of the Western countries, it would be disrespectful
to try and define death according to a specific spir-
Withholding and Withdrawal itual dogma. Moreover, when referring to death in a
of Treatment: Do Not Attempt critically ill patient, other issues, such as organ dona-
tion, come to mind. The Academy of Medical Royal
Resuscitation (DNAR) Orders Colleges has produced a ‘Code of practice for the
• Withholding treatment –not initiating treatment diagnosis and confirmation of death’ (2008).
due to no discernable benefit foreseen, usually in
irreversible clinical situations, for example not
offering vasoactive medication, intubation, renal
Brain-Stem Death
replacement therapy. The following are criteria for the diagnosis of death fol-
lowing irreversible cessation of brain-stem function.
• Withdrawing treatment –stopping ongoing
Prerequisites:
treatment because of no benefit detectable, for
example stopping inotropic support in refractory • Known aetiology of brain damage
end-stage cardiogenic shock with end-organ • Reversible causes of coma have been excluded
dysfunction. • No evidence of depressant drugs or residual
• Limitation of treatment (ceiling of treatment/no muscle paralysis
escalation) –occurs when the critical care team • Temperature >34 °C
are reluctant to make recommendations either • Exclusion of reversible circulatory, metabolic or
for withdrawal of treatment or for continuation endocrine disturbances
of full support; in the words of SA Murray (2008), • No reversible cause of apnoea.
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Brain-stem death tests: such as Spain, where organ donation is opted out of

• No pupillary response to light rather than opted into, the UK does not have any such
• No corneal reflex legislation at the time of writing this chapter. The UK
• No vestibulo-ocular reflex Donation Ethics Committee has published several
• Doll’s eyes reflex recommendations in 2014.
• No motor response to pain in the trigeminal
nerve distribution Donation after Brain Death (DBD)
• No gag reflex and no cough reflex This is organ donation which takes place after brain-
• Apnoea despite PaCO2 > 6 kPa with normal PaO2, stem death criteria have been met. It is also known as
in the absence of bicarbonate administration or heart-beating donation. These donors have provided
previous severe respiratory disease. the majority of transplanted organs since the inception
The test should be performed by at least two physi- of transplant surgery in the 1950s. However, due to a
cians who have been qualified more than 5 years and multitude of factors, the numbers of DBD are decreas-
are competent to conduct and interpret the test. Each ing. The consequence has been the rapid development
physician tests individually, and each set of tests is of donations after circulatory death (DCD).
repeated twice. The time of death is the time of the
first positive set of tests. There is no specific time Donation after Circulatory Death (DCD)
interval that should be left between the tests, provided This is organ donation which takes place after cardi-
the acid-base balance and PaCO2 have had time to orespiratory criteria of death have been met. It is also
normalise between examinations. known as non-heart beating donation. Though there
When appropriate or indicated, other investiga- have been cases of organ retrieval after unanticipated
tions should be performed in order to ascertain irre- death, such as patients presenting to the accident and
versible cessation of brain-stem function. However, emergency department, this practice is fraught with
the details of these are beyond the scope of this chapter. potential complications, not only ethical but also con-
cerning organ viability. More frequent is organ dona-
Cardiac Death tion following planned withdrawal of treatment in
The following diagnostic procedure is common: the ICU.
Whichever the pool of donors is considered, the
• Absence of mechanical cardiac function, as
guiding principles are the same.
confirmed by absent heart sounds and absent
central pulse on palpation for five minutes • If donation is likely, the matter should be fully
• Fixed and dilated pupils considered when caring for the patient.
• Absent corneal reflexes • Once it has been established that further care is
unlikely to benefit the patient and that, based
• Absent motor response to supra-orbital pressure.
on the patient’s known beliefs and values, they
In critical care these criteria may be supplemented by would be supportive of organ donation, this
the following: consideration should become fully part of their
• Asystole on a continuous ECG display care in the last days and hours of life; this includes
• Still heart on echocardiography invasive and pharmacological interventions that
• Absent pulsatile flow on intra-arterial pressure may benefit organs.
monitoring, provided the patient does not have a
ventricular assist device or VA ECMO in place.
Special Considerations in
Organ Donation Framework in Cardiothoracic Critical Care
Perhaps unlike other subspecialties of critical care, the
ICU –the UK Practice cardiothoracic ICU landscape has changed dramati-
Organ shortage is a growing issue all over the world cally in the last decade with the advent of extracor-
and significant efforts have been made by all parties poreal life support. Both extracorporeal membrane
concerned, both nationally and internationally, to oxygenation (ECMO) and ventricular assist devices
increase the donor pool. However, unlike countries have become relatively commonplace. It is also highly
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probable that the total artificial heart (TAH) tech- also accompanied by potentially prolonged suffering
nology will be perfected and will become accessible and, to some, is the harbinger of an undignified death.
in the near future. There are a number of questions It is, therefore, a procedure that should be under-
which arise. taken once extensive consultation amongst medical
1. What are the ethical implications of medical teams and with the patient’s family has happened.
practice in these new categories of patients? Unfortunately, this is usually not physically possible
2. What is the legal framework governing the within the timeframe, which may lead to very confus-
medical act? ing and ultimately sad situations.
3. (When) is the patient allowed to die?
4. How to diagnose death in the ‘bionic man’? Medical Negligence
The doctor owes the patient a duty of care. The
definition of a standard of care has the basis in the
Ethical and Legal Issues in ECMO Patients Bolam test, as well as the subsequent modifications
ECMO patients are perhaps the prototype of cardio- to the law. In the last two decades there have been
thoracic ICU patients that engender a flurry of dis- many published guidelines by the Royal Colleges,
cussions and ethical considerations given the limited the National Institute for Clinical Excellence (NICE)
nature of the support. and the Scottish Intercollegiate Guidelines Network
(SIGN) amongst others. Since the guidelines are
ECMO as a Bridge to Nowhere not and should not be anything else than a guide,
This has become an unfortunately common encounter the court of law and the GMC have been employing
in the modern cardiothoracic ICU. The patient who expert medical witnesses to advise on certain claims
has been on ECMO for days, or even weeks, and who of negligence. An expert medical witness is an expe-
has recovered function of most of the organs, includ- rienced, well- respected specialist in a particular
ing neurological integrity, poses a real ethical prob- field, who can inform and advise the jury on specific
lem. They cannot survive without ECMO, but there is aspects of care.
no way out, either because the patient is too debili- As a result of the flurry of well-publicised medical
tated to be a transplant candidate, or because of some scandals there has been the introduction of revalida-
other ongoing issue which was unbeknown at the time tion and relicensing for all practising doctors by the
of initiation of therapy. The decision to withdraw life GMC. The aim is to ensure that all medical practition-
support and the discussions with the patient and their ers are up to date and fit to practise. The results of the
family put the whole critical care team under signifi- revalidation process will probably be visible within the
cant emotional stress. next 3 to 5 years, once all doctors have been through
the process.
Organ Retrieval from an ECMO Patient
What to do if a doctor is accused of negligence?
The same principles governing the process of organ Runciman et al. (2003) suggest a possible
retrieval in the non-ECMO patient should be fol- approach when dealing with accidental harm in
lowed. However, if considering DBD, then considera- healthcare.
tion needs to be given as to how the apnoea test will be
performed. Whilst there are no specific guidelines at
present, several authors recommend reduction in the Research in Critical Care
sweep gas flow. Research is necessary for the advancement of knowl-
edge. But recent years have unfortunately also seen
ECPR some medical research disasters. We refer the reader
This involves placing the patient in cardiac arrest to the TGN 412 trial, which caused serious morbidity
on VA ECMO while waiting for the heart function in six healthy volunteers, or to the experimental treat-
to recover, assuming that the dysfunction is mainly ment with rGH in ventilator dependent ICU patients.
related to hibernation and stunning. The decision The Declaration of Helsinki, adopted by the Medical
should be made in a timely fashion, before multiorgan Research Council, makes the distinction between:
failure sets in. Based on the evidence so far though, • Clinical research –medical research combined
ECPR has not enjoyed the success anticipated. It is with patient care; the patient must receive the
16:33:17
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best care, or at least, not worse than conventional autonomy, beneficience, non- malfeasance and jus-
treatment; tice. For more details, the reader is referred to the
• Non-clinical research –biomedical research, Department of Health document on governance
which is conducted on healthy volunteers. arrangements for research ethics committees.
Consent Learning Points
The researcher has the obligation to obtain consent • The most commonly used ethical framework
from the participants in the study; the language of the in medicine is based on the four principles –
consent form must be clear enough to a 12 year old, autonomy, beneficience, non-malfeasance and
and the participants in the trial or their next of kin justice.
must be aware that they can withdraw from the trail at • The Mental Capacity Act establishes the general
any point, without any adverse consequence for their guidelines with regards to obtaining consent or
clinical care. applying treatment to patients who lack capacity.
• Approximately a third of the patients who die
Publication Ethics in intensive care have their treatment withheld
• Large trials are usually required to be registered or withdrawn, or have been subject to a
with one of the international registries in order to DNAR order.
avoid unnecessary duplication. • The diagnosis of death and the legal framework
• Plagiarism –passing the work of others as one’s governing organ donation determine UK practice;
own; this is a very serious offence, usually with they form the basis of transplant ethics.
significant repercussions from the GMC or other • Medical research is subject to constraints laid
national and international bodies. by the Research and Ethics Committee and the
• Fabricated data –intentional use of selective or Intellectual Property Law.
fictitious results of a trial; if the respective trial
is included in a meta-analysis, it can skew the Further Reading
results significantly and ultimately impact on
Academy of Medical Royal Colleges. A Code of Practice
patient safety.
for the Diagnosis and Confirmation of Death.
• Undisclosed conflicts of interest –recently, a London: Academy of Medical Royal Colleges, 2010.
number of significant, well-respected medical
Danbury C, Newdick C, Lawson A, Waldmann C (Eds).
research figures have been employed by the Law and Ethics in Intensive Care. Oxford: Oxford
medical industry as advisors on the development University Press, 2010.
of new drugs or technology. Unfortunately, there Department of Health. Governance Arrangements
have been cases where authors of significant for Research Ethics Committees. 2012. Available
trials in the recent past have failed to disclose the from: www.gov.uk
financial or other allegiances to the sponsoring Herring J. Q&A Medical Law, 3rd edition.
company; this resulted in the publication of London: Routledge, 2016.
fabricated data and had severe consequences for Murray SA, Sheikh A. Palliative care beyond cancer: care
all involved. for all at the end of life. British Medical Journal. 2008;
Most of those who have tried to initiate a medical 336: 958–959.
research project will be familiar with the Research and Roth P. Everyman. London: Jonathan Cape, 2006.
Ethics Committees. Such a committee is appointed to Runciman WB, Merry AF, Tito F. Error, blame, and the law
examine the research proposal and determine whether in health care –an Antipodean perspective. Annals of
it is ethical and whether it respects the standards of Internal Medicine. 2003; 138: 974–979.
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Training in Cardiothoracic Intensive Care

Chapter
57 Amy Needham and Chinmay Padvardthan
The hardest conviction to get into the mind of a begin- postoperative care after cardiac surgery. He employed
ner is that the education upon which he is engaged is cardiologists, an anaesthesiologist, a haematologist,
not a medical course, but a life course, for which the a neurologist, a nephrologist and a psychiatrist to look
work of a few years under teachers is but a preparation. after his first postoperative case of mechanical aortic
Sir William Osler The Student of Medicine valve replacement in 1960. He can be credited as the
trailblazer in the concept of cardiothoracic intensive
care. The first purpose built, 12 bed cardiac surgery
A Historical Perspective intensive care unit opened in 1964 at Broadgreen
From its nascence in the polio epidemic of Copenhagen Hospital in Liverpool. The catalyst for growth of
in 1952 to the foundation of the Faculty of Intensive intensive care units was the growing demands of open
Care Medicine in 2010, intensive care medicine has heart surgery, which increasingly required specialised
made great strides to become one of the fastest grow- haemodynamic and metabolic monitoring.
ing specialties in hospital medicine. The past 60 years Another important key change that influenced
have brought great technological advances in medi- future cardiac intensive care was the development
cal devices and we now have better understanding of of coronary care units (CCU) in 1961, dedicated to
critical illness pathologies. We have improved the care looking after patients with myocardial infarction and
processes in intensive care, implementing evidence addressing issues of arrhythmias and prompt resus-
based interventions such as low tidal volume venti- citation with closed chest compressions. In the late
lation, bundles of care and critical care outreach. We 1960s the second stage in the development of the
have introduced better predictors of risk and observed CCU was ushered in by Bernard Lown and colleagues
a reduction in mortality of the critically ill. in Boston, Massachusetts. They described a shift from
Developments and progress in anaesthesia and resuscitation at the time of an arrest to monitoring for
evolution of the concept of ‘intensive care units’ are early signs of clinical change and prevention of a car-
inexorably linked with the progress of cardiac surgery. diac arrest.
John H Gibbon Jr first successfully demonstrated the 1978 saw recognition of cardiac anaesthesia
use of a cardiopulmonary bypass machine to perform as an anaesthetic subspecialty in its own right in
open heart surgery in May 1953. Prior to this, cardiac North America with establishment of the Society of
surgery as we know today hardly existed. Surgeons Cardiovascular Anesthesiologists. It was not until
were almost warned against operating on the heart. In 1984 that the Association of Cardiac Anaesthetists
the words of Theodor Billroth, the famous Viennese (ACTA) came into existence in the UK. Dedicated
surgeon, ‘Any surgeon who attempts operating on the cardiac anaesthetists became a vital part of the ‘team’
heart should lose the respect of his colleagues’. Any looking after cardiac surgical patients in the postop-
cardiac surgery prior to Gibbon’s bypass machine was erative period. Over the past 40 years the post cardiac
mostly on cardiac trauma, and a few rheumatic mitral surgery care units evolved into the highly specialised
repairs. However, since 1953, great strides have been cardiothoracic intensive care units of the twenty-first
made in cardiac surgery and surgeons now routinely century.
perform a plethora of complex procedures. Albert From its humble beginnings, today’s cardiotho-
Starr was one of the early cardiac surgical pioneers racic intensive care unit (CTICU) is a highly complex
who adopted a multidisciplinary team approach to behemoth. At its heart are the highly trained specialist
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Chapter 57: Training in Cardiothoracic Intensive Care
intensivists, surgeons, cardiologists, specially trained in the UK and Australasia, however, took a different
nurses, pharmacists, dieticians, physiotherapists, per- pathway with intensive care medicine initially pre-
fusionists and technicians, all working together with dominantly being the domain of anaesthetists.
input from almost every medical and surgical specialty Australia and New Zealand introduced a com-
in the hospital. The patient population has expanded prehensive subspecialty training programme in criti-
from postsurgical patients, to include diverse patholo- cal care in 1996 with the formation of the College of
gies such as advanced heart failure, severe pulmonary Intensive Care Medicine in 2008. In the UK the Faculty
hypertension, mechanical circulatory support, extra- of Intensive Care Medicine was formally established
corporeal membrane oxygenation (ECMO) support, in 2010. The General Medical Council approved the
transplant patients and post cardiac arrest patients. standalone subspecialty training programme for criti-
CTICUs now provide long term respiratory wean- cal care medicine in 2012. The Canadians have a total
ing, tracheostomy care, renal replacement therapies, training requirement which is similar to the rest of
plasma apheresis, bronchoscopies and every other North America/Latin America (i.e. 5 years of spe-
form of therapeutic intervention offered on a general cialty training); but all base specialties agreed to a 2
intensive care unit. Globally there has been a shift in year critical care training programme following the
patient demographics. Patient case mix in intensive primary subspecialty training with a single conjoint
care units is increasingly elderly, with multiple comor- examination.
bidities such as diabetes mellitus, chronic airways Spain and Latin American countries also went
disease, hypertension and renal failure. The falling down the same route of requiring a minimum 5 years
incidence of fatal ST elevation myocardial infarc- of base specialty training. The European Society of
tion, on the other hand, has seen a rise in incidence Intensive Care Medicine (ESICM) was established
of complications associated with non- ST elevation in 1984 in Geneva to promote education, training
MI, and complications associated with mechani- and standardisation across Europe in intensive care.
cal support devices. These changes have altered the ESICM offers a Diploma in Intensive Care Medicine
natural history of cardiovascular illnesses and these (EDIC) to trainees from various specialties with 2
have started to resemble the natural history of criti- years of critical care experience.
cally ill patients on general intensive care units with
a greater incidence of multiorgan dysfunction requir-
ing organ support. The disease trajectory of a patient
Current Status of Intensive Care
admitted after a cardiac complication now resembles Medicine Training
that for any other critical illness, bringing with it the Since 2010, the Faculty of Intensive Care Medicine
complications of prolonged immobility, critical illness has been responsible for regulation and organisation
neuropathy, resistant infections, renal failure requir- of training in the specialty. A separate curriculum
ing prolonged support, need for specialist nutrition, was established for intensive care medicine training
issues with vascular access, chronic sepsis etc. This in 2011. Standalone intensive care medicine (ICM)
means there is a significant effect on resources, bed specialty training received the approval of the General
allocation and availability and in particular need for Medical Council in 2012.
specialist personnel training. Training in ICM in the UK is extensively modelled
This need for specially trained medical staff to look on the CoBaTriCE syllabus developed by the ESICM.
after the complex needs of the critically ill patients was The trainees are also expected to develop general pro-
first recognised in the USA. The first critical care resi- fessional knowledge, skills, attitudes and behaviours
dency was established at the Presbyterian University required of all doctors. These common competen-
Hospital, Pittsburgh in 1962 under the direction of cies in the core aspects of medical practice are iden-
Peter Safar. The residency was initially opened for tified from the Academy of Medical Royal Colleges
anaesthesiologists. However, subsequently it became Common Competencies.
open to different hospital specialties like surgery, The single specialty CCT training programme
internal medicine, paediatrics and pulmonology. Each in ICM lasts for 7 years; however in trainees in dual
specialty introduced a different pathway to get into CCT, training may extend for 8.5 years or more. Prior
the specialty, with each stipulating their own specific to starting ICM training, trainees need to have com-
requirements on training and experience. Training pleted a 2 year ICM core training programme. These
16:34:49 463
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include ‘Common stem programme’ in acute care block in a cardiothoracic intensive care unit during
common stem training (ACCS), which may include the second stage of their training. There are formal
trainees from acute medicine, emergency medicine, learning objectives that the trainees have to achieve by
common medical training (CMT) or core anaesthetic the end of the module. They are as follows:
training. Trainees are required to have passed the rel- • Be able to manage cardiac failure following an
evant stage of examinations in their specialty (first acute cardiac event;
part of the FRCA exam, full membership examination
• Be able to manage postoperative cardiac patients
of the College of Emergency Medicine). Competitive
following both elective and emergency cardiac
entry into a national specialty training programme is
surgery;
at the specialist trainee year 3 (ST3) level. Training
• Be aware of the indications for discussion and
progresses through three stages. The first stage of
transfer of critically ill patients to regional
higher specialist training lasts for 2 years and is aimed
cardiothoracic units;
at developing core competencies in intensive care.
For example, a trainee from an emergency medicine • Be able to stabilise and transfer patients with
background would achieve competencies in anaes- acute cardiorespiratory conditions requiring
thesia. These competencies are detailed in the ICM cardiothoracic intensive care.
curriculum. In the final 3 months of the second stage of training,
The second stage of training lasts 2 years, and additional experience can be gained in cardiothoracic
includes subspecialty training in various aspects of intensive care if a trainee wishes to do so.
intensive care such as paediatric intensive care, car- In the second stage of training, a trainee who
diothoracic intensive care etc. The second stage also wishes to specialise in cardiothoracic intensive care
includes a ‘specialist skills year’ where trainees are able may spend a year doing so. There also exists an oppor-
to pursue specialist interests such as echocardiogra- tunity to gain out of programme experience (OOPE)
phy, pre-hospital medicine, medical education and in the specialty. Thus a trainee coming out of a stan-
importantly cardiac intensive care. dalone ICM training programme may expect up to
The final year (final stage) is a mandatory year in 18 months of training in cardiothoracic intensive care.
intensive care medicine, where a trainee is expected But this programme does not allow the opportunity
to absorb management and non-technical skills in the for an in depth experience in anaesthesia or cardiac
run up to becoming a consultant. anaesthesia unless trainees decide to dual accredit.
The dual CCT training programme is possible The Royal College of Anaesthetists (RCoA) is
for trainees in acute medicine, respiratory medicine, responsible for provision of specialist training in
renal medicine, anaesthesia and emergency medicine. anaesthesia in the UK. The current specialty train-
This is again via a competitive recruitment process ing programme in anaesthesia is a 7 year programme,
and extends the duration of training depending on which mandates a minimum 9 months of ICM train-
the time taken for the competencies to be achieved. ing. In addition to this, the trainee in anaesthesia is
The Faculty of Intensive Care Medicine has laid out expected to gain 9 months of ‘spiral’ learning in car-
details of the competencies, practical skill sets and diac anaesthesia over the course of the programme
learning outcomes and assessment tools in its cur- at different stages, or 6 months of spiral learning and
riculum document. Australia and New Zealand have 12 months of specialist experience in the advance year
a similar structured specialty training programme in (year 6 or 7), in cardiothoracic anaesthesia. During
critical care medicine. this time, the trainee is expected to gain knowledge,
skills and experience of cardiothoracic anaesthesia,
echocardiography skills and principles of cardiotho-
Opportunities for Training in racic intensive care as required in the curriculum. The
Cardiothoracic Intensive Care majority of the current cohort of cardiothoracic inten-
In the UK, currently training in cardiothoracic intensivists in the UK, to this date, have been trained via
sive care is provided as part of the standalone inten- this route and only a few have a formal accreditation
sive care medicine training and anaesthesia. All in intensive care medicine. Anecdotally, many anaes-
intensive care medicine specialty trainees are cur- thetists pursue a further fellowship in cardiothoracic
rently expected to complete a mandatory 3 month anaesthesia, which includes cardiothoracic intensive
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Chapter 57: Training in Cardiothoracic Intensive Care
care built into it. This has traditionally been the train- care, adult cardiac and/or thoracic anaesthesia for a
ing and service provision model in cardiothoracic minimum of one year in recognised training centres
intensive care in the UK. However, there is no sepa- as part of general training. Those providing intensive
rate curriculum in cardiothoracic intensive care other care for cardiac surgical patients should have received
than the domains described in the CCT document. training to the minimum level as defined by the FICM
special skills year in cardiothoracic ICM’.
As a consequence of these regulations, and the
Training in Echocardiography gradual arrival of specialist ICM trained consultants
Training and formal qualification in transoesopha- in cardiothoracic intensive care on the scene, the tra-
geal echocardiography (TOE) has for many years ditional service provision model is going to change.
been a fundamental component of cardiothoracic Already there is a lively debate in the medical liter-
anaesthesia and intensive care and has seen an expo- ature on who is best placed to look after patients in
nential expansion in terms of clinical utility, support- cardiothoracic intensive care units. The European
ing guidelines, literature, expertise and enthusiasts. Society of Cardiology (ESC) Working Group for Acute
This familiarity with the modality of ultrasound and Cardiac Care has recommended that intensive cardiac
echo and availability of resources has enabled car- care units be directed by board certified cardiologists
diac anaesthetists and intensivists to rapidly adapt specially trained and accredited as acute cardiac care
the technology and lead the way in terms of using specialists, including training in the general inten-
ultrasound diagnostically in the intensive care unit. sive care unit. Recently, a leadership group within
A working group composed of members from the the American Board of Thoracic Surgery has recom-
Intensive Care Society (ICS) and the British Society mended development of a cardiothoracic critical care
of Echocardiography has developed a training certification pathway for the perioperative care of
scheme termed focused intensive care echo (FICE), cardiothoracic surgery patients. The American Heart
which aims to equip intensivists with a practical basic Association has also recognised the need for includ-
competency platform from which to develop further ing intensive care medicine in training and develop-
echo skills. This training programme has been well ing training pathways for cardiologists to train in
supported by cardiac anaesthetists and intensivists. cardiothoracic intensive care medicine. The Society of
Based on this simple and practical model, lung ultra- Cardiovascular Anesthesiologists has sought approval
sound is also developing as a bedside investigation in from the Accreditation Council for Graduate Medical
the ICU with protocols such as BLUE (bedside lung Education (ACGME) for accreditation of cardiotho-
ultrasound in emergency) and FALLS (fluid admin- racic anaesthesiology training as a new subspecialty.
istration limited by lung sonography) being incorpo- There have been attempts at creating a compre-
rated into daily clinical practice. Echocardiography hensive curriculum and described learning domains
remains a mainstay of cardiac perioperative care, and in cardiothoracic critical care training in the USA.
this unique concentrated exposure to echocardiog- Similar attempts have been made in the UK. A curricu-
raphy makes the CTICU a highly valuable training lum in cardiothoracic intensive care typically includes
experience. competencies in intensive care medicine, critically ill
cardiology patients (advanced heart failure), specialist
surgical skills (emergency sternotomy and manage-
Future of Cardiothoracic Intensive ment of postcardiac surgery cardiac arrest), echocar-
Care Training diography and ultrasound competencies, mechanical
Recently, the Intensive Care Society and Faculty of circulatory support, and extracorporeal membrane
Intensive Care Medicine (UK) published guidance on oxygenation support. Also included are competencies
the provision of intensive care in the UK. On this back- in end of life care, organ donation and provision of
ground, in 2015 the Royal College of Anaesthetists rehabilitation and support.
have published guidance on the provision of cardio-
thoracic anaesthesia and intensive care which states
that ‘Consultant anaesthetists intending to undertake Cardiac Intensivists in ACTA (CIA)
anaesthesia for cardiac or thoracic surgery should A subgroup of the already well-
established
have received training to higher level in adult intensive Association of Cardiothoracic Anaesthetists
16:34:49 465
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constituting elected consultant and trainee repre- It is inevitable that as medicine continuously evolves,
sentatives was recently established in the UK with an cardiothoracic critical care will become ever more
aim of raising the profile of cardiac intensive care as complex. The expectations of patients and regulators,
a specialty and of developing excellence in clinical financial pressures, change of patient demograph-
care through: ics and exponential increase in medical expertise will
• Setting standards for education, training and undoubtedly put pressure on current physician train-
clinical care provision; ing programmes to deliver a comprehensive training in
• Sharing data for benchmarking; cardiothoracic intensive care. So new ways of training
• Sharing clinical guidelines and best practice; will have to be created. If current evolution of critical
• Sharing innovation; care medicine into an independent specialty has taught
us anything, it is that it is only a matter of time! As the
• Involvement in guidelines produced by other
saying goes: All things are changing, and we are chang-
affiliated societies, for example ICS, FICM and
ing with them.
SCTS.
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Exercise Answers
Chapter 2 Particular care should be taken when withdrawing

the bronchoscope, especially in the case of fenes-
1. (d), 2. (c), 3. (b), 4. (b), 5. (a) trated tubes, to avoid shearing damage to the scope.
5. (d) Endobronchial stents are deployed either via rigid
Chapter 3 bronchoscopy or using an over-a-guidewire inser-
1. (a) True, (b) False, (c) False, (d) True, (e) False tion method using the fibreoptic scope to monitor
deployment.
2. (a) True, (b) False, (c) False, (d) False, (e) False
3. (a) False, (b) True, (c) True, (d) False, (e) True
Chapter 6
4. (a) True, (b) True, (c) True, (d) True, (e) True
1. False, 2. False, 3. True, 4. False, 5. False
5. (a) True, (b) True, (c) False, (d) True, (e) True
Chapter 7
Chapter 4 1. (a), 2. (d), 3. (b), 4. (a), 5. (d)
1. (d) Young patients at low risk do not need invasive
coronary angiography.
2. (b) Saline prehydration is most useful at preventing
Chapter 8
CIN. 1. (a) False, (b) True, (c) True, (d) False, (e) True
3. (d) Radial cases have longer screening times and 2. (a) False, (b) False, (c) False, (d) False
higher radiation doses than femoral cases. 3. (a) True, (b) False, (c) True, (d) False, (e) True
4. (c) Diagonal branches supply the anterolateral LV 4. (a) True, (b) True, (c) True, (d) True, (e) True
myocardium.
5. (a) True, (b) True, (c) False, (d) True, (e) False
5. (b) Load with dual antiplatelet therapy so that ad hoc
PCI can be performed if indicated. Intravenous fluid
at 500 ml/hour may cause pulmonary oedema and Chapter 9
make it difficult for the patient to lie flat for the pro- 1. (e), 2. (a), 3. (a), 4. (d), 5. (c)
cedure. Diuretics are usually omitted prior to angi-
ography as are oral anticoagulants.
Chapter 10
Chapter 5 1. (e), 2. (e), 3. (b), 4. (d), 5. (c)
1. (e) All of the above.

2. (c) Aspirin is not contraindicated in bronchoscopy.
Chapter 11
1. (c), 2. (d), 3. (c), 4. (a), 5. (a)
3. (d) A double lumen tube has a maximum outer
diameter of 4 mm which necessitates using a thin
adult or paediatric bronchoscope. Chapter 12
4. (a) When scoping through a tracheostomy, the inter- 1. (c) Tazocin and gentamicin would be the first choice
nal diameter (without inner tube) should be at least in this hypothetical situation. In practice, we would
2 mm greater than the bronchoscope outer diameter. give a combination of antibiotics to which the
16:37:22
468
Exercise Answers
patient responded clinically previously (e.g. ceftazi-

dime + meropenem etc.). It may be worth consid-
Chapter 19
ering nebulised colistin after discussing with the 1. (a) True, (b) False, (c) False
microbiologist. In case of severe sepsis, however, Nutritional assessment of patients is best done by
or known resistance to either of these antibiotics, simple and cheap screening tools including physical
meropenem would be a good second choice. All examination and screening questionnaires.
antibiotics, though, should be changed once cul-
2. (a) False, (b) False, (c) False
tures and sensitivities are back.
Energy intake is notoriously under reported by diary
2. (c) Note: It is important to take at least two sets of
entries. At energy balance, body weight will remain
blood cultures before giving antibiotics. Treatment
steady. BMR decreases with age as the body composi-
should be reviewed with culture results (blood cul-
tion changes with a loss of lean tissue.
tures and valve tissue if surgery is performed) and
modified accordingly. In case of a culture-negative 3. (a) False, (b) False, (c) True
endocarditis, atypical serology should be done and The critically ill patient has an increased protein
16/18S PCR considered. turnover causing loss of lean body mass. There is
3. (b) no evidence that anti-inflammatory drugs improve
protein metabolism in critically ill patients. Protein
4. (c) This patient is septic. Broad spectrum antibiotics
oxidation is often calculated from urinary nitrogen
should be started first, but take at least two sets of
excretion.
blood cultures first and a swab of pus if any, then
review with cultures. Duration for LVAD endocardi- 4. (a) False, (b) False, (c) True
tis (as it is probably in this case) –6 weeks but could Protein intake should exceed the recommended
be longer (e.g. until transplanted if surgery is immi- 0.8 g/kg/day for a healthy individual. A wide range
nent, if not, 6 weeks and stop, re-culture or give sup- of carbohydrate and fat should be administered at
pressive long-term treatment). 2–6 and 0.5–1.5 g/kg/day, respectively. This would
5. (a) need adjustment for individual patient clinical
requirements.
Chapter 13 5. (a) True, (b) False, (c) False

1. (c), 2. (a), 3. (a), 4. (c), 5. (e) Nasograstric feeding should be commenced after 24–
48 hours. There is no evidence suggesting gastric or
postpyloric placement of the feeding tube is superior.
Chapter 14 The volume of gastric aspirates should be assessed
1. (c), 2. (b), 3. (a), 4. (c) no data support any of the when commencing nasogastric feeding.
other statements in cardiac ICU patients, 5. (b)
Chapter 15 Chapter 20
1. (e), 2. (c), 3. (e), 4. (c), 5. (d)
1. (e), 2. (c), 3. (e), 4. (d), 5. (d)
1. (c), 2. (a), 3. (e), 4. (d), 5. (b) 1. (c), 2. (d), 3. (a), 4. (d), 5. (d)
1. (c), 2. (d), 3. (e), 4. (b), 5. (c) 1. (c), 2. (a), 3. (d), 4. (d), 5. (a)
1. (d), 2. (b), 3. (a), 4. (e), 5. (a)
1. (b), 2. (b), 3. (b), 4. (e), 5. (c)
16:37:22
469
Exercise Answers
1. (c), 2. (b), 3. (c), 4. (d), 5. (a) 1. (a) False, (b) False, (c) True, (d) False, (e) True
2. (a) False, (b) True, (c) True, (d) False, (e) True
Chapter 25A 3. (a) False, (b) False, (c) True, (d) False, (e) False
1. (e), 2. (d), 3. (c), 4. (b), 5. (d) 4. (a) False, (b) True, (c) True, (d) True, (e) False
5. (a) True, (b) False, (c) True, (d) False
Chapter 25B
1. (c), 2. (d), 3. (b), 4. (c), 5. (c) Chapter 37
1. (c), 2. (a), 3. (c), 4. (d), 5. (d)
Chapter 26
1. (b), 2. (d), 3. (c), 4. (c), 5. (e) Chapter 38
1. (d), 2. (c), 3. (d), 4. (b), 5. (b)
Chapter 27
1. (b), 2. (e), 3. (c), 4. (c), 5. (c) Chapter 39
1. (c), 2. (b), 3. (d), 4. (d), 5. (a)
1. (a), 2. (a), 3. (c), 4. (d), 5. (b)
1. (a), 2. (c), 3. (e), 4. (e), 5. (b)
1. (c), 2. (e), 3. (d), 4. (b)
1. (b), 2. (b), 3. (b), 4. (e), 5. (c)
1. (b), 2. (c), 3. (a), 4. (a), 5. (d) 1. (e), 2. (c), 3. (b), 4. (b), 5. (d)
1. (e), 2. (e), 3. (e), 4. (b), 5. (d) 1. (e), 2. (e), 3. (e), 4. (e), 5. (b)
1. (e), 2. (b), 3. (a), 4. (b), 5. (e) 1. (d), 2. (b), 3. (c), 4. (e), 5. (a)
1. (c), 2. (c), 3. (c), 4. (a), 5. (d) 1. (e), 2. (e), 3. (c), 4. (d), 5. (d)
1. (e), 2. (c), 3. (b), 4. (c), 5. (c) 1. (f), 2. (b), 3. (d), 4. (c)
1. (a), 2. (d), 3. (e), 4. (b), 5. (a) 1. (b), 2. (e), 3. (d), 4. (c), 5. (c)
16:37:22
470
Exercise Answers
1. (a) True, (b) False, (c) True, (d) True, (e) False 1. (b), (c), (d), 2. (d), 3. (a), (d), 4. (a), (b), (d), 5. (a),
2. (a) False, (b) False, (c) True, (d) True, (e) True (b), (e)
3. (a) False, (b) True, (c) False, (d) False, (e) True
4. (a) True, (b) True, (c) False, (d) False, (e) False
Chapter 52
1. (a) True, (b) False, (c) False, (d) True, (e) True
5. (a) False, (b) True, (c) True, (d) True, (e) False
2. (a) True, (b) True, (c) True, (d) False, (e) False
Chapter 49 3. (a) True, (b) True, (c) False, (d) False, (e) False
1. (a), 2. (d), 3. (b), 4. (e), 5. (e)

Chapter 55
Chapter 50 1. (c), 2. (a), 3. (b), 4. (c), 5. (d)
1. False, 2. False, 3. True, 4. False, 5. (a) 3, (b) 4, (c) 3,
(d) 1, (e) 2 (both iNO and sildenafil act via phospho-
diesterase 5 inhibition)
16:37:22
Index
More Information
471
Index
abdomen examination, 5 laboratory investigations, 368 adrenaline, see epinephrine

abdominal complications, 294 outcomes, 365 Advanced Directive (AD), 457
acalculous cholecystitis, 297 pathobiology, 365–67 advanced life support (ALS), 211–13
diverticulitis, 298 alveolar epithelial injury, 365–66 drugs, 213
gastrointestinal haemorrhage, 295–96 circulating cell role, 367 modifications, 213
incidence, 295 endothelial activation and non-VT/VF arrests, 213
mesenteric ischaemia, 296 injury, 366–67 pulseless VF/VT, 212
pancreatitis, 296–97 injured lung repair, 367 age, as risk factor, xxiv
perforations, 297–98 ventilator associated lung injury, 367 air leak, 360
prediction, 294 pharmacotherapy, 369 airway, 213–14
pseudo-obstruction, 297 prone positioning, 370 assessment, 59, 231
risk factors, 294 pulmonary oedema, 47 airway emergencies, 231
acalculous cholecystitis, 297 treatment strategies, 360 failed airway, 232–35
access site complications, 26 ventilator management, 368 can’t intubate, can’t ventilate
ACE inhibitors, 267, 377 PEEP, 368 (CICV), 233–35
active cycle of breathing technique protective ventilation, 368 obstruction, 231–32
(ACBT), 168 recruitment manoeuvres, 368 advanced airway management, 232
acute aortic syndrome, 45, 347–48 ventilatory modes, 368 assessment, 231
imaging studies, 45–47 acute respiratory failure (ARF), 247 causes, 231
acute coronary syndrome, imaging hypercarbic, 249–50 initial management, 232
studies, 45 decreased tidal ventilation, 250 postextubation, 238
acute hypercapnic respiratory failure, increased CO2 production, 249 organisational considerations, 238–39
ECMO, 205–6 increased dead space, 250 equipment, 238
acute kidney injury (AKI), 119, 120, hypoxaemic, 247–49 planning and preparation, 239
149, 154 diffusion abnormalities, 249 staff and training, 238
CABG patients, 314–15 inadequate alveolar oxygen, 247–48 postextubation emergencies, 237–38
complications, 151 increased venous admixture, 249 airway contamination, 238
ECMO patients, 199 shunt, 249 airway obstruction, 238
heart transplant patients, 336 ventilation and perfusion unplanned extubation, 237–38
nutritional implications, 162 mismatch, 248–49 tracheostomy emergencies, 235–37
paediatric surgery complications, 425 treatment, 253–54 airway bleeding, 237
pathogenesis, 120 ECMO, 254 blocked tube, 237
pulmonary endarterectomy patients, 329 inhaled vasodilators, 253 dislodgement, 237
acute lower limb ischaemia, 5 intubation and mechanical airway pressure release ventilation (APRV),
acute rejection, lung transplant ventilation, 253 145, 368
patients, 344 non-invasive positive pressure albumin, 117–19
acute respiratory distress syndrome ventilation (NIPPV), 253 alpha1 receptors, 123
(ARDS), 250, 365 prone positioning, 253 alpha2-adrenoceptor agonists, 134
cell therapies, 369 restrictive fluid strategy, 254 alveolar epithelial injury, 365–66
criteria, 251 supplemental oxygen, 253 Alzheimer dementia, 385
definition, 365 adenosine, 353 amiodarone, 213
ECMO, 203–5, 368 admission to critical care, xix, xxi amniotic fluid embolism, 413
less severe ARDS, 205 alternative resources, xx analgesia, 135
severe ARDS, 203–5 diagnostic and surgical-related delirium prevention, 396
following thoracic surgery, 359–60 factors, xix infusion pharmacokinetics, 130
general supportive measures, 369 fast-track approach, xx lung transplant patients, 344
imaging studies, 54 patient related factors, xix monitoring, 135
incidence, 365 timing, xx non-opioid analgesia, 137–39
471

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472
Index
analgesia (cont.) hypotension, 318 atelectasis

opioids, 136–37 hypovolaemia, 318 bronchoscopy applications, 30
planning, 135–36 ventricular assist device imaging studies, 52–53
regional analgesia, 139–40 complications, 189 thoracic surgery complications, 361
thoracic surgery, 357–59 aortic stenosis, 317 atrial fibrillation, 12
angiography, see coronary angiography postoperative problems, 318 following thoracic surgery, 361
angiotensin receptor blockers (ARBs), 377 arrhythmia, 318 mitral valve surgery patients, 320
antibiotics bradycardia, 318 prophylaxis, 362
administration in the critically ill, 95–97 hypertension, 318 risk factors, 361
appropriate antibiotic therapy, 95 hypotension, 318 treatment, 362
catheter related bloodstream stroke, 318 atrial flutter, 12
infections, 100–1 TAVI patients, 318 atrial septal defect, 430
endocarditis management, 98–100, 280 aortic surgery atrioventricular septal defect, 430
extracorporeal circuits and, 97–98 anaesthesia, 353–54 audit cycle, 446
historical background, 95 conditions requiring aortic Autoflow®, 143
implanted device infection surgery, 347 autonomy principle, 456
management, 98–100 critical care management, 349–52 AV block, 12
lung transplant patients, 341–42 aortic arch surgery, 350 AV node re-entrant tachycardia
prophylaxis, 328, 337 ascending aorta surgery, 350 (AVNRT), 13
resistance, 40, 102–3, 252, 282 descending aorta surgery, 351 AV re-entrant tachycardia (AVRT), 13
infective endocarditis, 100 intraoperative, 350 axillary cannulation, 196
multidrug resistant organisms, 103 monitoring, 350 azathioprine, 336
selective digestive decontamination preoperative, 349–50
(SDD), 281 stable patients, 350–52 Barlow’s disease, 319
susceptibility testing, 41 unstable patients, 349–50 basic life support (BLS), 211
therapeutic drug monitoring, 41 ICU goals, 352 bed rest effects, 164
anticoagulation, 24 coagulopathy management, 352 cardiovascular, 164
anticoagulant characteristics, 153 haemodynamics, 352 neuromuscular, 164
anticoagulant reversal, 114 spinal cord protection, 352 psychological, 164
bleeding complications, 307 aortic valve surgery, 317–18 respiratory, 164
cardiac ECMO patients, 198 anatomical considerations, 317 bedside nurse, 441–42
chronic thromboembolic pulmonary common ICU problems, 318 Behavioural Pain Scale (BPS), 135
hypertension patients, 326, 329 physiological considerations, 317–18 beneficience, 456
heart failure management, 378 APACHE score, xxv benzodiazepines, 133–34, 396
heparin resistance, 403–4 aprotinin, 310 Bernard Soulier disease, 403
heparin induced thrombocytopenia argatroban, 405, 406 best interests, 457
patients, 405 arm examination, 4 beta receptors, 123
bivalirudin, 405 arrhythmias, 77. See also specific beta-blockers, 266, 377
renal replacement therapy, 153–54 arrhythmias bidirectional Glenn procedure, 423
valve surgery patients, 321 aortic stenosis patients, 318 bilirubin levels, xxv
ventricular assist device implantation, 186 CABG patients, 315 biphasic positive airway pressure
antiepileptic drugs (AEDs), 291–92 grown-up congenital heart disease, 429 (BIPAP), 145
antifungals, 102 paediatric, 420 bivalirudin, 405
antimicrobial stewardship, 103 cardiac surgery complications, 424 bleeding, 307–8, 402. See also
antimicrobials. See antibiotics pregnant patients, 415 haematological disorders
antiplatelet agents, 24 thoracic surgery complications, 361–62 CABG patients, 315
platelet transfusion and, 108 arterial catheters, 87–88. See also causes, 307
antithrombin, 404 vascular access compression of structures by clot, 307
aorta. See also thoracic aortic indications, 87 following thoracic surgery, 363
aneurysm (TAA) information from the arterial pulmonary haemorrhage, 330
echocardiography, 19 waveform, 88 transfusion algorithms, 308
injury, 304–5 pulse pressure variation, 88 blood conservation, 114
trauma, 349 arterial waveform, 88 blood cultures, 39
aortic dissection, 19, 45, 270, 347–48, 349 Aspergillus infections, 102 blood pressure. See also hypertension;
chest pain, 243 aspiration mean arterial pressure (MAP)
classification, 347 imaging studies, 53 autoregulation, 263
traumatic, 304 risk factors, 53 blood products, 107–11
aortic regurgitation, 317 aspirin, 321 allogenic product administration, 308–9
combined valvular pathologies, 321 CABG patients, 315 cryoprecipitate and fibrinogen
postoperative problems, 318 assist-control ventilation (AC), 145 concentrate, 110
472

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473
Index
fresh frozen plasma, 110 Candida infections, 102 cardiac tamponade, 17, 244

platelets, 108–10, 309 can’t intubate, can’t ventilate paediatric, 422, 424
prothrombin complex, 110 (CICV), 233–35 cardiac transplantation. See heart
recombinant FVIIa, 111 oxygen delivery techniques, 233–35 transplantation
red blood cells, 107–8 rescue techniques, 233 cardioembolism, 19
blood transfusion. See also blood products capnography, 214, 239 cardiogenic shock, 256, 372. See also shock
algorithms, 308 carbohydrate, 160 causes, 193
side effects, 108 cardiac arrest, 19. See also resuscitation ECMO indications, 193. See also
transfusion coagulopathy, 309 causes, 213 cardiac ECMO
body composition measurement, 157 non-VT/VF arrests, 213 imaging studies, 47–48
Bolam test with the Bolitho out-of-hospital arrest, 220 neonatal, 419
amendment, 457 early percutaneous coronary cardiopulmonary bypass (CPB), 215,
bowel ischaemia, 5, 6 intervention, 224 350, 352
brachial plexus injury, 383 family screening, 228 neurological complications, 380–81
bradycardia, 213 haemodynamics, 224–25 risk reduction, 381
aortic stenosis patients, 318 intensive care management, 222 pregnant patients, 415
causes, 77–78 mechanical circulatory cardiorenal syndrome, 372–73
hypothermia response, 226 support, 226–27 cardiorespiratory disease symptoms, 1
when to pace, 78 organ donation, 227–28 cardiothoracic imaging, 44
brain injury following cardiac oxygen therapy, 225 acute aortic syndrome, 45–47
arrest, 458–59 practical approach, 224 acute coronary syndrome, 45
brainstem death, 459 prognostic issues, 226 acute respiratory distress
BRiSc score, xxv survival, 220 syndrome, 54
bronchoalveolar lavage, 30 targeted temperature aspiration, 53
bronchopleural fistula, 31, 360–61 management, 225–26 atelectasis and collapse, 52–53
imaging, 54 ventilation, 225 cardiogenic shock, 47–48
bronchopneumonia, 53 withdrawal of cardiorespiratory chest pain, 45
bronchoscopy, 28 support, 226 chest X-ray, 44
complications, 35 persistent precipitating pathology, 222 computed tomography, 44–45
contraindications, 31–32 postcardiac arrest brain injury, 458–59 pericardial tamponade, 48
indications, 28 postcardiac arrest myocardial pleural effusion, 51
atelectasis management, 30 dysfunction, 221 pneumonia, 53
haemoptysis diagnosis and postcardiac arrest syndrome, 220–21 pneumothorax, 51
management, 30 systemic ischaemia/reperfusion pulmonary embolus, 48
immunocompromised patients, 30 response, 222 pulmonary oedema, 47
intubation, 28–29 cardiac death, 459 respiratory emergencies, 50
persistent bronchopleural fistula, 31 cardiac ECMO, 193. See also extracorporeal right ventricular failure, 48
respiratory infection diagnosis in membrane oxygenation (ECMO) surgical complications, 49–50
ventilated patient, 29–30 cannulation strategies, 194–96 trauma and surgery associated
thoracic trauma, 30–31 axillary/subclavian cannulation, 196 desaturation, 54
physiological effects, 31 carotid artery cannulation, 196 ultrasound, 44
preparation, 32–34 central cannulation, 196 cardiothoracic trauma. See trauma
equipment, 32 femoral artery cannulation, 194–95 cardioversion, 82
patient, 32 peripheral cannulation, 194 special considerations, 82–83
personnel, 33 circuit design, 194 carotid artery cannulation, 196
precautions, 34 complications, 199 catheter insertion, 86. See also arterial
ventilation and oxygenation contraindications, 194 catheters; central venous catheters;
options, 34 future directions, 199–200 pulmonary arterial catheter
procedure, 35 general patient management, 196–98 complications, 86
procedures performed, 31 indications, 193–94 pregnant patients, 409
with conscious sedation, 34 outcomes, 199 catheter related bloodstream
with general anaesthesia, 34–35 weaning, 434 infections, 100–1
bundle branch block, 12 cardiac injuries, 304 central line associated bloodstream
bundle of His, 317 cardiac intensivists in ACTA (CIA), 465–66 infections (CLABSI), 100–1, 282
bundles of care, 445 cardiac output prevention strategies, 282
low output following paediatric cardiac central venous catheters, 88–89. See also
calcineurin inhibitors, 337, 343 surgery, 420 vascular access
side effects, 387 mechanical ventilation effects, 147 central pressures, 89
calcium channel blockers, 266, 412 monitoring, 90–91 central venous pressure trace, 89
calcium sensitisers, 126–27 cardiac power output (CPO), 374 CentriMag system, 181
473

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Index
cerebrospinal fluid drainage, 352–53 extracorporeal carbon dioxide removal superior cavopulmonary

Chelsea Critical Care Physical Assessment (ECCO2R), 206 connection, 423
tool (CPAx), 167 lung transplantation, 342–43 total cavopulmonary connection, 423
chest compressions, 211 management, 252, 253 consent issues, 456–58
chest drainage, 357 ventilator complications, 205 best interests, 457
complications, 74–75 chronic thromboembolic pulmonary coronary angiography, 23
chylothorax, 75 hypertension (CTEPH), 273, 324 deprivation of liberty, 458
drain malposition, 74 cerebrovascular issues, 329 medical research, 461
heart injury, 74 clinical presentation, 325 patients who have capacity, 457
infection, 75 critical care management, 326–27 patients who lack capacity, 457
intercostal vessel injury, 74 drugs, 328 constrictive pericarditis, 18
nerve injuries, 74 fluid balance, 329 continuous mandatory ventilation
oesophageal perforation, 75 haematology, 329 (CMV), 144
re-expansion of pulmonary monitoring, 327–28 continuous positive airway pressure
oedema, 74 ventilation, 328 (CPAP), 145, 170
contraindications, 73 diagnosis, 325 continuous renal replacement therapy
historical background, 70 medical management, 325–26 (CRRT), 151
indications, 70 pathophysiology, 324 heart transplant patients, 336
nursing care, 73 pulmonary endarterectomy, 326 continuous venovenous haemofiltration
procedure, 70–73 residual pulmonary (CVVH), heart failure patients, 378
anatomical landmarks, 70 hypertension, 329–30 contrast complications, 26
patient positioning, 71 surgical treatment, 324 contrast induced nephropathy (CIN), 23
preinsertion preparation, 71 chylothorax, 75, 425 coronary angiography, 22
removal of drains, 74 ciclosporin, 337 complications, 25–26
underwater seals, 73 circumflex artery, 319 access site complications, 26
chest electrodes, 7 citrate anticoagulation, 153 contrast complications, 26
chest pain, 241 clinical audit, 446 major adverse cardiac events
aortic dissection, 243 clinical effectiveness, 446–47 (MACE), 26
cardiac tamponade, 244 clinical governance, 446 consent, 23
differential diagnosis, 241 clinical guidelines, 445 haemostasis and postprocedural care, 24
examination, 241 clinical information systems (CIS), 449 historical perspective, 22
gastrointestinal causes, 245 components of, 449–52 image acquisition, analysis and
history, 241 costs and benefits, 452–54 interpretation, 24
imaging studies, 45 effects on clinical practice, 454–55 indications, 22
myocardial ischaemia, 242–43 clonidine, 134 preprocedural assessment, 22–24
postpercutaneous coronary Clostridium difficile, 39 access site preparation, 23
intervention, 242 coagulopathy. See also haemostasis allergy and adverse reaction
postsurgical revascularisation, postoperative tests, 111–14 history, 23
242–43 laboratory tests, 113–14 anticoagulation, 24
myocardial rupture, 244 point-of-care testing, 114 antiplatelet agents, 24
myocarditis, 244 preoperative screening, 111 arterial access route, 22–23
pericarditis, 244 cognitive decline, 385 prehydration, 23
superior vena cava syndrome, 243 colloid solutions, 116–17 premedication, 23
Takotsubo cardiomyopathy, 245 community acquired pneumonia coronary artery bypass grafting
tension pneumothorax, 244 (CAP), 252 (CABG), 313
vascular air embolism, 243–44 compartment syndrome, 26 graft occlusion prevention, 315
wound pain and sternal dehiscence, 245 computed tomography (CT), 44–45, 389 haemodynamic management, 313–14
chest reopening, 215 pregnant patients, 410 patient population, 313
outside the ICU, 216 congenital heart disease, 413–14, 418–22 postoperative complications, 315
chest wall trauma, 302 adult. See grown-up congenital heart acute kidney injury, 314–15
chest X-ray, 44 disease (GUCH) myocardial infarction, 314
pregnant patients, 410 incidence, 418 postsurgical chest pain, 242–43
children. See paediatrics presentations, 418–20 prevention, 388
cholecystitis, 245 arrhythmias, 420 coronary artery disease in
acalculous, 297 cardiogenic shock, 419 pregnancy, 414–15
chronic lung allograft dysfunction cyanosis, 418 corticosteroids, 280, 336
(CLAD), 344 heart failure and failure to thrive, 420 antenatal, 412
chronic obstructive pulmonary disease pulmonary oedema, 420 cough assist, 170
(COPD), xxiv, 252–53 univentricular circulations, 422 creatinine levels, xxiv, xxv
acute exacerbations, 252 initial palliation, 422 cricoid pressure, 61
474

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Index
cricothyroidotomy, 63, 233 difficult intubation, 28–29, 62–63 limb electrodes, 7

critical care, xix predictors, 59 precordial (chest) electrodes, 7
Critical Care Pain Observation Tool diffusion abnormalities, 249 pregnant patients, 409
(CPOT), 135 distributive shock, 256 QRS axis estimation, 11
cryoprecipitate, 110 diuretics, 267 QRS transition, 11
crystalloid solutions, 116–17, 119 heart failure management, 375 rhythm, 10
cyanosis diverticulitis, 298 waves and intervals, 9–10
grown-up congenital heart disease, 428 Do Not Attempt Resuscitation (DNAR) J point, 9
neonatal, 418 orders, 458 P wave, 9
management, 419 DO2/VO2 mismatch, 257 PR interval, 9
cystic fibrosis, 343 dobutamine, 123–24, 275 QRS complex, 9
cytomegalovirus heart failure management, 376 QT interval, 9
lung transplant patients, 342 dopamine, 125, 275 ST segment, 9
prophylaxis in heart transplant patients, 337 heart failure management, 376 T wave, 9
dopexamine, 126 U wave, 9
daily sedation interruption (DSI), 132 dyspnoea, 247. See also acute respiratory electroencephalography (EEG), 286–88
damping, 87 failure (ARF) delirium investigation, 398
dashboarding, 447 chronic thromboembolic pulmonary failure to awaken management, 389
dead space, 250 hypertension, 325 seizure diagnosis, 285
death COPD, 252–53 therapeutic monitoring, 292
brainstem, 459 pneumonia, 252 electronic medical records, 451
cardiac, 459 pneumothorax, 250–51 electronic test ordering, 38
diagnosis of, 458 pulmonary oedema, 251–52 encephalopathy, 382–83
deep breathing exercises (DBEx), 168 endocarditis. See infective endocarditis
deep venous thrombosis, 5 early rehabilitation, 165 endotracheal intubation. See intubation
pregnant patients, 415 Early Warning Scores (EWS), 215 endovascular stent graft, 349
defibrillation, 82, 211. See also implanted Ebstein’s anomaly, 431 energy balance, 157
cardiac devices echocardiography energy expenditure, 158
pulseless VT/VF, 212 heart failure monitoring, 374 energy intake, 157
special considerations, 82–83 indications, 15–19 enhanced recovery programs, 357
delirium, 392 aorta, 19 enoxaparin, 329
core features, 392 cardiac arrest, 19 enoximone, 377
diagnosis, 397–99 haemodynamic monitoring, 19 enteral nutrition, 160–61
examination, 398 intracardiac masses, 19 composition of feeds, 161
history, 397–98 intracardiac shunts, 19 contraindications, 160
investigations, 398–99 left ventricle, 15–17 reference daily intakes, 161
incidence and prevalence, 393 pericardium, 17–18 epileptiform activity, 292
mechanisms, 393 pulmonary embolism, 19 epinephrine, 124–25, 213, 377
negative clinical consequences, 392 right ventricle, 17 epsilon aminocaproic acid (EACA), 309
prevention strategies, 394–97 trauma, 19 ethics principles, 456
general non-pharmacologic valvular heart disease, 17 autonomy, 456
interventions, 396–97 pregnant patients, 409 beneficience, 456
perioperative interventions, 395–96 procedural guidance, 20 justice, 456
postoperative interventions, 396 shock patients, 258, 259–60 non-malfeasance, 456
preoperative screening, 394–95 training, 465 European Association of Cardiothoracic
risk factors, 393 transoesophageal (TOE), 15 Surgery (EACTS) guidelines, 211
screening, 397 transthoracic (TTE), 15, 224 EuroSCORE, xxiv
subtypes, 393 focused scanning, 15 everolimus, 337
treatment, 399 education team, 441 examination
depression, 395 ejection fraction (EF), 16 abdomen, 5
deprivation of liberty, 458 electrocardiography (ECG), 7 chest pain, 241
desmopressin, 310–11 12 lead ECG, 8 conscious patient, 4–5
dexmedetomidine, 135 bipolar limb leads, 8 general inspection, 4
diagnostic imaging. See cardiothoracic ECG arrangement, 8 hands and arms, 4
imaging; specific imaging techniques precordial leads, 8 legs, 5
diaphragmatic injury, 305 unipolar augmented limb leads, 8 modification for use in critical care, 1
diaphragmatic paralysis, 425 axis, 11 neck, 4–5
diarrhoea, 39 calibration, 7 praecordium, 5
diazepam, 133 filter settings, 7 pregnant patients, 409
differential lung ventilation, 146–47 heart rate, 10 unconscious patient, 5–6, 224
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exercise testing, pregnant patients, 409 failure to thrive, 420 arrhythmias, 429

exponentially weighted moving average fat, 160 endocarditis, 430
(EWMA) charts, 447 femoral artery cannulation haemoptysis, 430
extracorporeal carbon dioxide removal complications, 194–95 heart failure, 429
(ECCO2R), 202 fentanyl, 136 surgical/postoperative
COPD, 206 fibrinogen, 110 admissions, 430–32
extracorporeal cardiopulmonary replacement, 110 atrial septal defect, 430
resuscitation (eCPR), 193, 218 fibrinolysis, 309–10 atrioventricular septal defect, 430
ethical and legal issues, 460 flexible bronchoscopy. See bronchoscopy congenitally corrected transposition of
out-of-hospital arrest management, 226 fluid administration, 116 the great arteries, 431
Extracorporeal Life Support Organisation albumin, 117–19 Ebstein’s anomaly, 431
registry, 199 colloids vs crystalloids, 116–17 Fontan and Fontan-type
extracorporeal membrane oxygenation crystalloid solutions, 119 circulations, 432
(ECMO), 202, 215 fluid responsiveness, 121 systemic-pulmonary shunt, 431
acute respiratory failure, 254 hydroxyethyl starch (HES), 119 tetralogy of Fallot, 431
cannulation configurations, 203 hypertonic solutions, 119 transposition of the great arteries, 431
cardiac failure management. See indications, 116 guidelines, 445
cardiac ECMO pathophysiology, 116 Guillain–Barré syndrome (GBS), 385
complications, 5 sepsis patients, 279
ethical and legal issues, 460 fluid balance management, 119–20. See also haematological disorders, 402. See also
organ retrieval, 460 fluid administration bleeding
future directions, 207 lung surgery patients, 120 congenital disorders, 402–3
heart transplant patients, 335 pulmonary endarterectomy patients, 329 haemophilia, 402
indications, 203–7 fluid responsiveness, 19 inherited platelet disorders, 403
acute hypercapnic respiratory evaluation, 259 von Willebrand’s disease, 402–3
failure, 205–6 shock patients, 258–59 heparin resistance, 403–4
acute respiratory distress syndrome follow-up, 443–44 heparin induced thrombocytopenia
(ARDS), 203–5, 368 Fontan and Fontan-like circulations, 432 (HIT), 404–5
lung transplantation, 206 forced expiration technique (FET), 168 haemodiafiltration, 149
primary graft dysfunction (PGD), 206 fresh frozen plasma, 110 haemodialysis, 149
pulmonary vascular disease, 206–7 Full Outline of UnResponsiveness (FOUR) haemodynamic monitoring, 19
lung transplant patients, 344 score, 388 haemofiltration, 149
microbiological testing, 38 fungal infections, 102. See also infections haemophilia, 402
suggested testing set, 39 lung transplant patients, 342 haemoptysis
paediatric, 423–24 bronchoscopy applications, 30
platelet transfusion, 109 G protein coupled receptors (GPCR), 123 grown-up congenital heart disease
principles, 202 mechanism of action, 123 patients, 430
pulmonary endarterectomy patients, 330 Gastrointestinal Complications Score haemorrhage. See bleeding
respiratory physiotherapy, 171 (GICS), 294–95 haemostasis. See also coagulopathy
therapeutic drug monitoring, 41 gastrointestinal haemorrhage, 295–96 cardiopulmonary bypass effects, 111
extravascular lung water index lower GI bleed, 295–96 diagnostic testing, 111
(EVLWI), 92 upper GI bleed, 295 haemothorax, 301
extubation, 63–64, 237 gender, as risk factor, xxiv CABG patients, 315
controlled, 29 general anaesthesia, bronchoscopy, 34–35 hand examination, 4
delay, 435 genetic testing in pregnancy, 415 health care support worker, 442
postextubation emergencies, 237–38 gestational hypertension, 410 heart block, CABG patients, 315
airway contamination, 238 Glanzmann’s thrombasthenia, 403 heart failure, 180, 372
airway obstruction, 238 global end-diastolic volume index causes, 372
unplanned extubation, 237–38 (GEDVI), 92 clinical presentation, 372
protocols for early extubation, 434 glyceryl trinitrate, 412 ECMO application, 193. See also
role of checklists and prompts, 435 Gott shunt, 352 cardiac ECMO
screening parameters for early grown-up congenital heart disease endocarditis, 280
extubation, 434 (GUCH), 427 grown-up congenital heart disease, 429
ICU management, 427–29 infants, 420
factor XII deficiency, 403 cyanotic patient, 428 investigations, 373
failed ventilation, 63, 232–35 failing morphological right management, 374–75
can’t intubate, can’t ventilate ventricle, 429 drug therapy, 375–77
(CICV), 233–35 general principles, 427–28 intra-aortic balloon pump, 378
oxygen delivery techniques, 233–35 univentricular heart, 429 intubation, 375
rescue techniques, 233 indications for ICU admission, 429–30 non-invasive ventilation, 375
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oxygenation, 375 hydralazine, 376, 412 infection, 281

treatment goals, 374 hydroxyethyl starch (HES), 119 antibiotic therapy, 98–100
ultrafiltration, 378 hypercarbia, 249 magnet mode, 82
monitoring, 373–74 hypercarbic respiratory failure, 249–50 precautions when performing
venricular assist device decreased tidal ventilation, 250 procedures, 80–81
complications, 187–88 increased CO2 production, 249 removal, 281
heart injury in chest drainage, 74 increased dead space, 250 troubleshooting, 81–82
heart rate, 10 hypertension, 263 incentive spirometry, 168
heart rhythm, 10 acute, 265 indeterminate axis, 12
heart transplantation, 180, 333 aetiology, 263–64 indirect calorimetry, 158, 160
complications, 334 aortic stenosis patients, 318 induction agents, 337
acute cellular rejection, 336 classification, 264 infants. See paediatrics
frequency, 387 diagnosis, 264–65 infections, 38, 278. See also antibiotics;
neurological complications, 385–87 management, 265–67 microbiological testing; specific
prevention and risk assessment, 388 medications, 267 infections
contraindications, 333 perioperative, 266–67 central line associated bloodstream
discharge from critical care unit, 337 postoperative, 267 infections, 100–1, 282
patient transfer from operating preoperative, 265–66 chest drainage complications, 75
room, 333 pathophysiology, 263–64 fungal infections, 102
postoperative care, 333–37 pregnant patients, 410–12 general clinical management,
airway and ventilation, 334 postpartum care, 412 279–80
antimicrobial prophylaxis, 337 pulmonary. See pulmonary hypertension heart transplant patients, 387
cardiovascular, 334–35 hypertensive crisis, 270 prophylaxis, 337
immunosuppression, 336–37 hypertensive emergency, 265 implanted cardiac devices, 98–100,
renal, 336 hypertensive urgency, 265 281
preoperative assessment, 333 hypertonic solutions, 119 lung transplant patients, 341–42
HeartWare HVAD, 182 hypertrophic cardiomyopathy, 413 bacterial, 341–42
HELLP syndrome, 411 hypoperfusion, 257. See also shock fungal, 342
heparin, 153, 310, 321. See also signs of, 258 viral, 342
anticoagulation hypoplastic left heart syndrome mechanical circulatory support device
protamine effect, 310 (HLHS), 422 infections, 101–2
resistance, 403–4 hypotension, 257, 279. See also shock recognition of, 278–79
heparin induced thrombocytopenia aortic regurgitation patients, 318 screening for resistant organisms, 40
(HIT), 404–5 aortic stenosis patients, 318 surgical site, 282–83
diagnosis, 404 hypothermia, therapeutic, 381. See targeted thoracic surgery complications, 361
ICU management, 406 temperature management (TTM) ventricular assist devices, 188, 281
laboratory testing, 404 hypoventilation, 247–48 infective endocarditis, 4, 17, 280–81
management of patients for hypovolaemia, 273 antibiotic therapy, 98–100, 280
surgery, 405–6 aortic regurgitation patients, 318 diagnosis, 98
antibody positive, 405 hypovolaemic shock, 256 grown-up congenital heart disease
bivalirudin, 405 hypoxaemic respiratory failure, 247–49 patients, 430
treatment, 405 diffusion abnormalities, 249 patients at high risk, 98
hepatobiliary complications, 296–97 inadequate alveolar oxygen, 247–48 inferior vena cava diameter, 19
acalculous cholecystitis, 297 increased venous admixture, 249 inflammation
pancreatitis, 296–97 shunt, 249 lung, 367
high flow nasal oxygen therapy, 147 ventilation and perfusion resolution, 367
high frequency nasal oxygen (HFNO), 170 mismatch, 248–49 steroid treatment, 369
high frequency ventilation (HFV), 146 informed consent. See consent issues
high frequency oscillatory ventilation idiopathic pulmonary fibrosis, 343 infusion pharmacokinetics, 130
(HFOV), 368 iloprost, 276 inotropic agents. See also specific drugs
high thoracic epidural analgesia imaging. See cardiothoracic imaging heart failure management, 376
(HTEA), 139 immunocompromised patients, 30 intensive care, 457
historical perspectives, 462–63 immunosuppression intensive care unit acquired weakness
history, 1 lung transplantation, 343 (ICU-AW), 385
chest pain, 241 pharmacological side effects, 387 intermittent positive pressure ventilation
conscious patient, 1–3 Impella device, 175–76, 182 (IPPV), 169
modification for use in critical care, 1 implanted cardiac devices, 77. See also intermittent renal replacement therapy
pregnant patients, 409 ventricular assist devices (VAD) (IRRT), 151
unconscious patient, 3–4, 224 implantable cardioverter defibrillators International Liaison Committee on
Homan’s sign, 5 (ICDs), 79 Resuscitation (ILCOR), 220
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intra-aortic balloon pump (IABP), laryngospasm, 238 lung disease as risk factor, xxiv

173–75, 335 left anterior descending artery (LAD), 24 lung injuries, 303
alternative insertion routes, 174 left anterior hemiblock (LAHB), 12 lung rest strategy, 205
CABG patients, 313 left axis deviation, 12 lung torsion, postoperative, 54
complications, 174 left bundle branch block (LBBB), 12 lung transplantation, 340
duration and weaning, 174–75 left circumflex artery (LCx), 24 chronic obstructive pulmonary
heart failure management, 378 left main coronary artery (LMCA), 24 disease, 342–43
indications, 174 left posterior hemiblock (LPHB), 12 cystic fibrosis, 343
timing, 173 left ventricle echocardiography, 15–17 drug interactions, 343
intracardiac shunts, 19 left ventricular assist device (LVAD), 180 ECMO applications, 206, 344
intracranial haemorrhage, 382 complications, 187–89 general ICU issues, 340
intrathoracic blood volume index aortic regurgitation, 189 idiopathic pulmonary fibrosis, 343
(ITBVI), 92 device failure, 189 indications, 340
intravascular fluid. See fluid administration infections, 188 infections, 341–42
intubating laryngeal mask airway, 63 neurological complications, 188 bacterial, 341–42
intubation, 59–64 postoperative bleeding, 187 fungal, 342
acute respiratory failure, 253 right heart failure, 187–88 viral, 342
airway assessment, 59 thrombosis, 188 late admissions to ICU, 344
bronchoscopy and, 34 contraindications, 185 mobilisation, 344–45
bronchoscopy applications, 28–29 first generation, 181 primary graft dysfunction, 340–41
changing endotracheal tubes, 29 future directions, 189–90 pulmonary hypertension, 343
controlled extubation, 29 implantation risk factor lysine analogues, 309–10
difficult, 28–29, 62–63 assessment, 184–85
predictors, 59 cardiac factors, 184 macrocirculation, 256
double lumen tube placement, 29 echocardiography, 184 macronutrients, 160
extubation, 63–64 indications, 182 carbohydrate, 160
failed ventilation, 63 outcome, 189 fat, 160
heart failure patients, 375 functional status, 189 protein, 160
indications, 59 quality of life, 189 magnesium sulphate, 412
management of the intubated patient, 63 survival, 189 toxicity, 412
preparation, 59–61 patient selection, 184 magnetic resonance imaging (MRI), 389
drugs, 60 perioperative management during pregnant patients, 409
equipment, 60 implantation, 185–87 major adverse cardiac events (MACE), 26
patient, 60 ICU and ward care, 186 mandatory minute ventilation
sequence of events, 61–62 preoperative planning, 185 (MMV), 145
confirmation of correct position, 62 VAD team, 186–87 manual hyperinflation (MHI), 169
cricoid pressure, 61 self care, 187 manual insufflation exsufflation, 170
laryngoscopy, 61 left ventricular diastolic dysfunction mass spectrometry, 42
preoxygenation, 61 (LVDD), 17 Maze procedure, 320
team, 61 left ventricular dysfunction mean arterial pressure (MAP), 263
trauma patients, 301 as risk factor, xxiv phenylephrine effect, 127
invasive monitoring, 185 mitral valve surgery patients, 320 target, 224
inversed ratio ventilation (IRV), 145 left ventricular end-diastolic area mean frontal axis, 11
isoproterenol, 125 (LVEDA), 20 mechanical chest compression devices
left ventricular outflow tract (LVOT) (MCCDs), 226
J point, 9 obstruction, 17 mechanical circulatory support (MCS),
jugular venous waveform, 4 velocity-time integral (VTI), 20 173, 180. See also ventricular assist
junctional ectopic tachycardia (JET), 424 left ventricular systolic function (LVSF), 15 devices (VAD)
justice, 456 ejection fraction (EF), 16 contraindications and complications, 183
fractional shortening (FS), 16 device comparisons, 176
ketamine, 139 leg examination, 5 device infections, 101–2
Kussmaul’s sign, 5 levetiracetam, 292 heart transplant patients, 335
levosimendan, 126, 275 Impella device, 175–76
labetolol, 412 heart failure management, 377 intra-aortic balloon pump
labour management, 414 LiDCO system, 92 (IABP), 173–75
lacerations, lung, 54 lidocaine toxicity, 35 out-of-hospital arrest management, 225,
lactate levels, 257 limb electrodes, 7 226–27
Lance–Adams syndrome (LAS), 290 limitation of treatment, 458 paediatric, 423–24
laryngeal view, 62 lorazepam, 134, 291 TandemHeart device, 176
laryngoscopy, 61 lung collapse, imaging studies, 52–53 temporary, 180–81
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CentriMag system, 181 mesenteric ischaemia, 296 myoclonic status epilepticus (MSE), 290

indications, 180–81 metabolisable energy, 157, 158 myoclonus, 290
types of, 181 methylene blue, 128
mechanical ventilation, 142. See also methylprednisolone, 336 nasogastric feeds. See enteral nutrition
weaning from mechanical microarray technology, 42 neck examination, 4–5
ventilation microbiological testing, 38 negligence, 460
acute respiratory failure, 253 antibiotic susceptibility testing, 41 neonates. See also congenital heart disease;
cardiac ECMO patients, 198 liaison with infection specialists, 42 paediatrics
heart transplant patients, 334 microscopy and culture, 40–41 arrhythmias, 420
modes, 143, 144–45 new technologies, 41 cardiogenic shock, 419
airway pressure release ventilation mass spectrometry, 42 cyanosis, 418
(APRV), 145 microarrays, 42 management, 419
assist-control ventilation (AC), 145 molecular testing, 41 pulmonary oedema, 420
biphasic positive airway pressure sequencing, 42 nerve injuries in chest drainage, 74
(BIPAP), 145 ordering tests, 38 nesiritide, heart failure management, 376
continuous mandatory ventilation results interpretation, 42 neurally adjusted ventilatory assist
(CMV), 144 sampling procedures, 38–40 (NAVA), 146
continuous positive airway pressure screening for resistant organisms, 40 neurological complications, 380
(CPAP), 145 surgical samples, 40 brachial plexus injury, 383
intermittent positive pressure therapeutic drug monitoring, 41 cardiopulmonary bypass, 380–81
ventilation (IPPV), 169 microcirculation, 256 risk reduction, 381
mandatory minute ventilation midazolam, 133 cognitive decline, 385
(MMV), 145 milrinone, 125–26, 377 considerations with cardiac surgery, 380
pressure support ventilation (PSV), 145 mitral regurgitation, 318, 319 encephalopathy, 382–83
selection of, 144 combined valvular pathologies, 321 failure to awaken management, 388–89
synchronised intermittent mandatory mitral stenosis, 318, 319, 320 clinical assessment, 388
ventilation (SIMV), 145 mitral valve, 319 neuroimaging, 389
physiology, 147–48 calcification, 319 neurophysiologic investigations, 389
cardiovascular effects, 147 repair, 321 optic neuropathies, 383
respiratory effects, 147–48 systolic anterior motion (SAM), 321 peripheral nervous system, 383–85
principles, 143–44 mitral valve surgery, 318–20 prevention, 388
pressure control ventilation, 144 anatomical considerations, 318–19 stroke, 381–82
pressure regulated volume controlled common ICU problems, 320 transplantation related
ventilation (PRVC), 143 atrial fibrillation, 320 complications, 385–87
volume control ventilation, 143 left ventricular dysfunction, 320 neuromuscular blockade, 140
prolonged. See weaning from mechanical right ventricular dysfunction, 320 neutrophils, 367
ventilation ventilatory failure, 320 nitrates, heart failure management, 376
protective ventilation, 147 pysiological considerations, 319–20 nitric oxide, 276, 422
pulmonary endarterectomy patients, 328 mobilisation, 167–68 non-convulsive seizures (NCS), 285, 290
special modalities, 145–47 lung transplant patients, 344–45 non-convulsive status epilepticus (NCSE),
differential ventilation, 146–47 modelling. See risk models 285, 290, 383
high frequency ventilation (HFV), 146 molecular testing, 41 non-invasive ventilation (NIV), 147, 170
inversed ratio ventilation (IRV), 145 morphine, 136 See also ventilation
neurally adjusted ventilatory assist MRSA screening, 40 acute respiratory failure, 253
(NAVA), 146 mTOR inhibitors, 337 heart failure management, 375
non-invasive ventilation (NIV), 147 multidisciplinary teams, 445–46 role in difficult weaning from mechanical
technical aspects, 142 multidrug resistant organisms (MDR), 103 ventilation, 435–36
cycling phase, 142 Multiplate platelet function assay, 114 weaning failure, 438–39
limiting phase, 142 Mustard/Senning procedure, 431 non-malfeasance, 456
triggering phase, 142 mycophenolate mofetil (MMF), 336 norepinephrine, 124, 275, 377
variables, 143 myocardial infarction nursing team, 441–43
expiration, 143 CABG patients, 314 advanced nursing roles, 443
inspiration, 143 chest pain, 242–43 bedside nurse, 441–42
ventilator hyperinflation (VHI), 170 post percutaneous coronary education team, 441
weaning from. See weaning from intervention, 242 health care support worker, 442
mechanical ventilation postsurgical revascularisation, 242–43 hierarchy, 442
medical emergency teams (MET), 216 following thoracic surgery, 363 lead nurse, 442
medical negligence, 460 imaging studies, 45 matron, 442
Mental Capacity Act, 2005, 457 myocardial rupture, 244 nurse manager, 442
mesenchymal stem cells (MSCs), 369 myocarditis, 244 shift leader, 443
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nutritional assessment, 157 pancreatitis, 296–97 postoperative pulmonary complications

nutritional requirements, 157–59 parenteral nutrition, 161–62 (PPCs), 167. See also respiratory
energy balance, 157 patient preparation physiotherapy
energy expenditure, 158 bronchoscopy, 32 post-transplantation lymphoproliferative
energy intake, 157 chest drainage, 71 disorder (PTLD), 387
in disease, 159–60 intubation, 60 PR interval, 9
penetrating injuries. See trauma praecordium examination, 5
obstructive shock, 256 peptic ulcer, 295 precordial electrodes, 7
oedema, 5 perforated, 298 pre-eclampsia, 410
oesophageal injury, 305 percussion, 168 diagnosis, 410
perforation, 297 percutaneous coronary intervention (PCI) severe pre-eclampsia, 411
in chest drainage, 75 recommendations, 224 pregnancy, 408
oesophageal rupture, 245 pericardial tamponade, 4 amniotic fluid embolism, 413
openness, 447 imaging studies, 48 arrhythmias, 415
opioids analgesia, 136–37 pericarditis, 244 cardiopulmonary bypass, 415
optic neuropathies, 383 pericardium, echocardiography, 17–18 cardiovascular changes, 408–9
organ donation, 227–28, 459 peripartum cardiomyopathy, 408, 413 congenital heart disease, 413–14
donation after brain death, 459 peritoneal dialysis, 149 coronary artery disease, 414–15
donation after circulatory death, 459 phenylephrine, 127–28, 275 counselling and genetic testing, 415
ECMO patients, 460 phenytoin, 291 CVD diagnosis, 409–10
orotracheal intubation. See intubation phosphodiesterase (PDE) inhibitors, 377 history and examination, 409
outcome measures, 166–67 phrenic nerve, 383 deep vein thrombosis, 415
outreach, 443 injury, 425 hypertensive disorders, 410–12
oxycodone, 136 physical examination. See examination postpartum care, 412
oxygen therapy, acute respiratory physical functional intensive care test hypertrophic cardiomyopathy, 413
failure, 253 (PFIT), 166 labour management, 414
physiotherapy. See rehabilitation; peripartum cardiomyopathy, 413
P wave, 9 respiratory physiotherapy prehydration, coronary angiography, 23
pacing PiCCO system, 91–92 premedication, coronary angiography, 23
complications, 80 pimobendan, 126 preoxygenation, 61
implant complications, 80 plasmin, 309 pressure control ventilation, 144
implantable cardioverter defibrillators platelets, 108–10, 309 pressure monitoring, 86–87
(ICDs), 79 inherited platelet disorders, 403 central pressures, 89
pacemaker functioning, 78 pleural drainage. See chest drainage damping, 87
pacemaker magnet mode, 82 pleural effusion, 70 resonance, 87
pacemaker types, 79 chylous effusion, 425 transducers, 86–87
pacing mode, 78–79 imaging studies, 51 zeroing, 87
pacing threshold, 78 ultrasound assessment, 44 pressure regulated volume controlled
troubleshooting, 81–82 pleural space, 70 ventilation (PRVC), 143
when to pace, 78 pneumonia, 252 pressure support ventilation (PSV), 145
paediatrics community acquired, 252 preterm labour, 414
circulation assessment, 418 following thoracic surgery, 361 primary graft dysfunction (PGD), 206,
complications, 424–25 imaging studies, 53 340–41
acute kidney injury, 425 interstitial, 53 procalcitonin (PCT), 278
arrhythmias, 424 lobar, 53 prognosis, xxiii. See also risk models
cardiac tamponade, 424 ventilator associated (VAP), 147, proliferation inhibitors, 336
chylothorax, 425 281–82 prone positioning, 253, 370
neurological complications, 425 diagnosis, 29–30 propofol, 134
phrenic nerve injury, 425 reduction strategies, 281 propofol infusion syndrome (PRIS), 134
residual lesions, 424 pneumothorax, 70, 244, 250–51, 360 prostacyclin, 276
congenital heart disease, 418–22 imaging studies, 51 prosthetic valve endocarditis, 99
presentations, 418–20 spontaneous, 250 protamine, 310
mechanical circulatory support, 423–24 treatment, 251 protein, 160
postoperative care following cardiac positive end expiratory pressure prothrombin complex, 110, 114
surgery, 420–22 (PEEP), 144 protocols, 445
pulmonary circulation and ARDS patients, 368 pseudo-obstruction, 297
hypertension, 422 postcardiac arrest brain injury, 458–59 publication issues, 461
tamponade, 422 postcardiac arrest myocardial pulmonary artery catheter, 89–91
univentricular circulations, 422 dysfunction, 221 cardiac output monitoring, 90–91
pain, 135. See also analgesia; chest pain postcardiac arrest syndrome, 220–21 components, 90
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evidence base, 91 QRS axis estimation, 11 respiratory quotient (RQ), 159

heart failure monitoring, 374 QRS complex, 9 resting metabolic rate, 158
historical background, 89 QRS transition, 11 restrictive cardiomyopathy, 18
indications, 90 QT interval, 9 restrictive fluid strategy, 254
insertion, 90 resuscitation. See also advanced life support
measurements, 90 radial artery, post procedural care, 24 (ALS); basic life support (BLS)
pulmonary capillary wedge pressure Rastelli procedure, 431 catheter laboratory arrests, 218
(PCWP), 272 recombinant activated factor VIIa, 111, 311 general ward, 215–18
pulmonary contusions, 54 recruitment manoeuvres, 368 guidelines, 211
pulmonary embolism, 19 recurrent laryngeal nerve, 384 incidence, 211
ECMO applications, 206 red blood cells, 107–8 late resuscitation, 215
imaging studies, 48 regional analgesia, 139–40 rib fractures, 302
pulmonary endarterectomy (PEA), 273, regional wall motion abnormalities Richmond Agitation-Sedation Scale
324, 326 (RWMA), 16, 17 (RASS), 131, 397
complications, 329–30 rehabilitation right axis deviation, 12
pulmonary haemorrhage, 330 adjuncts and treatment, 165–66 right bundle branch block (RBBB), 12
reperfusion lung injury, 329 aims, 164–65 right coronary artery (RCA), 24
right ventricular failure, 329–30 barriers, 167 right dominant circulation, 24
critical care management, 326–27 early, 165 right ventricle (RV) echocardiography, 17
cerebrovascular issues, 329 outcome measures, 166–67 right ventricular assist device (RVAD),
drugs, 328 practicalities and safety issues, 166 180, 188
fluid balance, 329 remifentanil, 137 right ventricular dysfunction
haematology, 329 renal dysfunction, xxiv grown-up congenital heart disease, 429
monitoring, 327–28 renal replacement therapy (RRT), 149 heart transplant patients, 335
ventilation, 328 anticoagulation, 153–54 treatment, 335
operative principles, 326 discontinuation, 154 right ventricular failure, 17, 188
outcomes, 330 dose, 152–53 following thoracic surgery, 363
patient selection, 326 indications, 149, 151–52 imaging studies, 48
surgical techniques, 326 monitoring, 154 mitral valve surgery patients, 320
pulmonary haemorrhage, 330 nutritional implications, 162 pulmonary endarterectomy
pulmonary hypertension, 272–73, 325 outcome, 154 patients, 329–30
See also chronic thromboembolic timing, 151 right ventricular index of myocardial
pulmonary hypertension (CTEPH) types of, 149–51 performance (RIMP), 184
aetiology, 273 reperfusion lung injury, 329 risk factors
diagnosis, 325 reperfusion response, 222 postoperative, xxv
ECMO support, 206, 207 research and development, 448 circulatory, xxv
lung transplantation, 343 ethical and legal issues, 460 gastrointestinal/hepatic, xxv
medical therapy, 275–76 consent, 461 neurological, xxv
catecholamines, 275 publication issues, 461 renal, xxv
dobutamine, 275 resonance, 87 respiratory, xxv
levosimendan, 275 respiratory distress, 4 preoperative, xxiv–xxv
pulmonary vasodilators, 276 respiratory muscle training, 171 age, xxiv
vasopressin, 275 respiratory physiotherapy, 167–70 disease extent, xxiv
vasopressors, 275 active cycle of breathing technique gender, xxiv
monitoring, 274 (ACBT), 168 left ventricular function, xxiv
paediatric, 422 breathing exercises, 168 lung disease, xxiv
resuscitation, 274–75 cardiac patients, 171 previous surgery, xxiv
supportive care, 273 ECMO patients, 171 renal disease, xxiv
treatment of underlying causes, 273 incentive spirometry, 168 type of surgery, xxiv
pulmonary oedema, 251–52, 253, 372 indications, 167 risk management, 447
See also chest drainage intermittent positive pressure ventilation risk models, xxiii–xxv
imaging studies, 47 (IPPV), 169 postoperative, xxiii, xxv
neonatal, 420 manual hyperinflation (MHI), 169 risk factors, xxv
re-expansion, 74 manual insufflation exsufflation, 170 preoperative, xxiii–xxv
pulmonary thromboendarterectomy manual techniques, 168 risk factors, xxiv–xxv
(PTE), 207 mobilisation, 167–68 thoracic surgery, xxv
pulmonary torsion, 54 positioning, 168 rocuronium, 60
pulmonary vascular disease, ECMO respiratory muscle training, 171
applications, 206–7 thoracic surgery patients, 171 saline solution, 119
pulse pressure variation, 88 ventilator hyperinflation (VHI), 170 sampling procedures, 38–40
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scoring systems, xxiii. See also risk models sildenafil, 276 targeted temperature management
sedation, 130–31 single lung ventilation, 146–47 (TTM), 225–26
alpha2-adrenoceptor agonists, 134 sirolimus, 337 physiological responses, 226
benzodiazepines, 133–34 SOFA score, xxv tension pneumothorax, 74, 244
bronchoscopy, 34 somatosensory evoked potentials tetralogy of Fallot, 431
clonidine, 134 (SSEPs), 389 thoracic aortic aneurysm (TAA), 348–49
dexmedetomidine, 135 spinal cord drainage, 352–53 endovascular stent graft, 349
infusion pharmacokinetics, 130 sputum samples, 40 medical management, 349
monitoring, 131 ST segment, 9 open surgery, 348–49
planning, 131–33 standardised mortality ratio (SMR), 447 thoracic endovascular aortic repair
propofol, 134 status epilepticus, 285 (TEVAR), 353. See also aortic
Sedation-Agitation Scale (SAS), 131 myoclonic (MSE), 290 surgery
seizures, 285 stem cell therapies, 369 thoracic expansion exercises (TEEs), 168
burden of, 285–86 sternal closure, delayed, 422 thoracic injury. See trauma
causes and prognostic sternal dehiscence, 245 thoracic surgery, 356. See also aortic
significance, 288–90 steroid therapy, 369 surgery
post cardiac arrest, 290 stool samples, 39 complications, 363
post cardiac surgery, 288–90 stroke, 381–82 acute respiratory distress
diagnosis, 285 aortic stenosis patients, 318 syndrome, 359–60
general intensive care risk factors, 388 air leak and pneumothorax, 360
considerations, 290–91 ventricular assist device atelectasis, 361
management, 291–92 complications, 188 bleeding, 363
paediatric, 425 subclavian cannulation, 196 bronchopleural fistula, 360–61
prophylaxis with pre-eclampsia, 412 suctioning, 170, 281 cardiac dysfunction, 361–63
transplant patients, 387 superior cavopulmonary connection, 423 infections, 361
versus epileptiform activity, 292 superior vena cava (SVC), 20 mortality, 356
selective antegrade cerebral perfusion superior vena cava syndrome (SVCS), 243 reduction of mortality and
(SACP), 351 supraventricular arrhythmias, 12–13 complications, 356–59
selective digestive decontamination surgical samples, 40 analgesia, 357–59
(SDD), 281 surgical site infections, 282–83 enhanced recovery, 357
sepsis, 290. See also infections management, 283 pleural drainage, 357
definition, 278 prevention strategies, 283 thromboprophylaxis, 359
general clinical management, 279–80 Surviving Sepsis Campaign, 279 video assisted thoracic surgery
identification, 278 suxamethonium, 60 (VATS), 356
ventricular assist device swallowing, with tracheostomy, 66 risk modelling, xxv
complications, 188 synchronised intermittent mandatory thoracotomy, 357
septic shock, 256 ventilation (SIMV), 145 indications, 304
sequencing technologies, 42 Syntax score, xxiv pain control, 344
sequential organ failure score (SOFA), 278 systemic inflammatory response syndrome Thoratec HeartMate 3, 182
serotonin release assay (SRA), 405 (SIRS), 222 thrombocytopenia, 111
serum creatinine. See creatinine levels systemic vascular resistance (SVR), 123, thromboelastography (TEG), 114
shivering, hypothermia response, 226 258 thromboprophylaxis, 359
shock systemic-pulmonary shunt, 431 thrombosis
cardiogenic, See cardiogenic shock systolic anterior motion (SAM), 321 deep venous, 5, 415
definition, 256 management, 321 ventricular assist device
diagnosis, 257–58 predisposing factors, 321 complications, 188
distributive, 256 total cavopulmonary connection, 423
epidemiology, 257 T wave, 9 tracheobronchial injuries, 303
hypovolaemic, 256 tachyarrhythmias, 12–13 tracheobronchial tears, 54
monitoring, 258–60 heart transplant patients, 334 tracheoinnominate artery fistula, 237
ECG, 259–60 paediatric, 420 tracheostomy, 64–66, 233
fluid responsiveness, 258–59 cardiac surgery complications, 424 advantages, 64
obstructive, 256 supraventricular, 12–13 bronchoscopy and, 34
pathophysiology, 256–57 ventricular, 13 complications, 237
septic, 256 tacrolimus, 337 decannulation, 66
therapeutic strategies, 260–61 side effects, 387 emergencies, 235–37
shunt Takotsubo cardiomyopathy, 245 airway bleeding, 237
intracardiac, 249 tamponade. See cardiac tamponade blocked tube, 237
intrapulmonary, 249 TandemHeart device, 176 dislodgement, 237
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indications, 64 univentricular circulation, 422 definition, 282

insertion technique, 65 grown-up congenital heart disease, 429 diagnosis, 29–30
percutaneous, 65 initial palliation, 422 reduction strategies, 281
surgical, 65 superior cavopulmonary connection, 423 ventilator hyperinflation (VHI), 170
management, 66 total cavopulmonary connection, 423 ventricular arrhythmias, 13
percutaneous, 233 urine samples, 40 ventricular assist devices (VAD), 180
swallowing and, 66 See also mechanical circulatory
timing, 65–66 valproate, 292 support (MCS)
tubes, 64–65 valve surgery patients, 317 complications, 187–89
cuffed and uncuffed, 64 aortic valve, 317–18 aortic regurgitation, 189
fenestrated and non-fenestrated, common ICU problems, 318 device failure, 189
65 combined valvular pathologies, 321 infections, 102, 188
single and double cannula, 65 implant considerations, 321 neurological complications, 188
weaning protocol, 66 choice of prosthesis, 321 postoperative bleeding, 187
training mitral valve, 318–20 right heart failure, 187–88
current status, 463–64 common ICU problems, 320 thrombosis, 188
echocardiography, 465 postoperative anticoagulation, 321 components, 180
future of, 465 tricuspid valve, 320–21 Impella, 175–76
historical background, 463 valvular heart disease, implantable/durable devices, 79
opportunities, 464–65 echocardiography, 17 indications, 182
tramadol, 139 vascular access, 86 patient selection, 184
tranexamic acid (TXA), 290, 309–10 arterial catheters, 87–88 types of, 181–82
transducers, 86–87 cardiac ECMO cannulation strategies, implantation risk factor
zeroing, 87 194–96. See also cardiac ECMO assessment, 184–85
transposition of the great arteries, 431 catheter insertion, 86 cardiac factors, 184
congenitally corrected, 431 catheter related bloodstream ECG assessment, 184
transpulmonary dilution and pulse contour infections, 100–1 infection, 281
analysis, 91–92 central venous catheters, 88–89 outcome, 189
LiDCO system, 92 complications, 86 perioperative management during
non-calibrated systems, 92 pressure monitoring, 86–87 implantation, 185–87
PiCCO system, 91–92 pulmonary artery catheter, 89–91 ICU and ward care, 186
transpulmonary gradient (TPG), 185 vascular air embolism, 243–44 preoperative planning, 185
trauma, 301 vasoactive receptors, 123 VAD team, 186–87
aortic injury, 304–5 vasodilators, 253, 276, 369 self care, 187
bronchoscopy indications, 30–31 heart failure management, 375 ventricular fibrillation, pulseless, 212
cardiac injuries, 304 vasopressin, 127, 213, 275 ventricular tachycardia (VT), pulseless, 212
cardiothoracic trauma mechanisms, vasopressors, 275 ventriculoarterial (VA) coupling, 257
301 venoarterial carbon dioxide difference video assisted thoracic surgery
chest wall, 302 (pCO2 gap), 258 (VATS), 356
clinical assessment, 301 venoarterial ECMO, 202 videolaryngoscopy, 62
desaturation, imaging studies, 54 venovenous ECMO, 202, 203 viral infections. See also infections
diaphragmatic injury, 305 ventilation, 213–14. See also mechanical lung transplant patients, 342
echocardiography indications, 19 ventilation volume control ventilation, 143
imaging, 301–2 ARDS patients, 368 von Willebrand factor (vWF), 311
lung injuries, 303 protective ventilation, 368 von Willebrand’s disease, 402–3
oesophageal injury, 305 ventilatory modes, 368
thoracic aorta, 349 decreased tidal ventilation, 250 warfarin, 32, 321, 329
tracheobronchial injuries, 303 during bronchoscopy, 34 weaning from mechanical ventilation, 434
tricuspid annular plane systolic excursion failed, 63 difficult weaning, 435
(TAPSE), 184 heart transplant patients, 334 extubation delay, 435
tricuspid regurgitation, 17, 185, 320 out-of-hospital arrest management, 225 non-invasive ventilation role, 435–36
tricuspid valve, 320 ventilation and perfusion (V/Q) role of checklists and prompts, 435
surgery, 320–21 mismatch, 248–49 protocols for early extubation, 434
tropomyosin, 126 ventilator associated lung injury screening parameters for early
troponin C (TnC), 126 (VALI), 147 extubation, 434
acute respiratory distress syndrome, 367 simple weaning, 434–35
U wave, 9 burden of, 368 weaning failure, 436–39
ultraprotective ventilation, 205 ventilator associated pneumonia (VAP), asssociated factors, 436–37
ultrasound imaging, 44 147, 281–82 data from clinical studies, 439
483

Index
More Information
484
Index
weaning from mechanical multidisciplinary team approach, 438 withholding treatment, 458

ventilation (cont.) non-invasive ventilation role, 438–39 Wolff–Parkinson–White syndrome
environment normalisation, 438 specialised weaning unit role, 436 (WPW), 13
gas exchange normalisation, 437 trials of unsupported breathing, 438 wound pain, 245
identification of causes, 437–38 weaning to most appropriate level, 439 wound swabs, 40
impact of prolonged mechanical Wilson’s central terminus, 8 written consent for coronary
ventilation, 436 withdrawing treatment, 458 angiography, 23
484

Core Topics in Cardiothoracic Critical Care

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Cambridge University Press

978-1-107-13163-7 — Core Topics in Cardiothoracic Critical Care

Core Topics in Cardiothoracic

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Core Topics in Cardiothoracic

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University Printing House, Cambridge CB2 8BS, United Kingdom

Cambridge University Press is part of the University of Cambridge.

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Section 1 – Diagnosis 9 Chest Drainage 70

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18 Renal Replacement Therapy 149 30 Systemic Hypertension in Cardiothoracic

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Section 7 – Disease Management 52 Difficult to Wean from Mechanical

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Darryl Abrams Peter A Barry

Jason M Ali Marius Berman

Joseph E Arrowsmith Paolo Bosco

Nicholas A Barrett Pedro Catarino

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Sumit Chatterji Simon J Finney

Max S Damian Jo-anne Fowles

Peter Faber Lisen Hockings

Shakil Farid Charles W Hogue

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Stephen P Hoole Jerrold H Levy

Anna Kydd Alia Noorani

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Erik Ortmann Alastair Proudfoot

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Mark Toshner Alain Vuylsteke

Steven SL Tsui Niki Walker

Kamen Valchanov Ian Welsby

Matt Varrier Vasileios Zochios

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Preface to the Second Edition

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Link between Cardiothoracic Anaesthesia and Intensive

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Which Patients are Admitted to Critical Care?

Table 1 Levels of critical care

Level of Criteria for admission Examples

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Which Patients are Admitted to Critical Care?

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Scoring Systems and Prognosis

Crystal Balls • Helping to measure the performance of the

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Scoring Systems and Prognosis

measurement and probably contributed to the dra- Extent of Cardiac Disease

Left Ventricular Function Renal Disease

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Scoring Systems and Prognosis

Other Risk Factors Renal

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Scoring Systems and Prognosis

Table 1 Postoperative cardiac surgery risk assessment scores

Organ system SOFA APACHE

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Scoring Systems and Prognosis

Nashef, SAM, Roques F, Sharples LD, et al. EuroSCORE

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AC Assist-Control ventilation BLUE Bedside Lung Ultrasound in

25 mm/s. This results in 10 second recording. Each –90°

VW = 1/3 (RA + LA + LL). aVF +90°

Intracardiac Shunts (McConnell’s sign), peak TR jet velocity >2.7 m/s and

Sequencing organisms detected from non-sterile sites require a